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In the diagnosis of a given disease it is essential that 
the physician rest his opinion not upon one or tivo symptoms, 
but upon a series of symptoms which when properly prat 
together give him a complete, cr nearly complete, picture of 
the malady. It is as futile for a physician to attempt to 
base a diagnosis upon one symptom as for an architect to 
attempt to determine the appearance of a house by seeing 
one of the stones which has been removed from its walls. 



PRACTICAL DIAGNOSIS 



THE USE OF 



SYMPTOMS AND PHYSICAL SIGNS IN 
THE DIAGNOSIS OF DISEASE 



UY 

HOBART AMORY HARE, M.D., B.Sc. 

PROFESSOR OF THERAPEUTICS IN THE JEFFERSON MEDICAL COLLEGE OF PHILADELPHIA; 

PHYSICIAN TO THE JEFFERSON MEDICAL COLLEGE HOSPITAL; ONE TIME CLINICAL 

PROFESSOR OF DISEASES OF CHILDREN IN' THE UNIVERSITY OF PENN81 I A \MA; 

LAUREATE OF THE MEDICAL SOCIETY OF LONDON, OF THE ROYAL 

ACADEMY i>1 MEDICINE IN BELGIUM; AUTHOR OF A TEXT-BOOK 

OF PRACTICAL rHERAPEUTIOS AND A TEXT-BOOK OF 

THE PRACTICE OF MEDICINE. 



SIXTH EDITION, REVISED AND ENLARGED 



ILLUSTRATED WITH 203 ENGRAVINGS AND 16 PLATES 




LEA BROTHERS & CO. 

PHILADELPHIA AND NEW YORK 

1907 



.jofiARY of CONGRESS 
l*o Cooles Received 

SEP 12 I90f 



ixc,, id, 

COPY B. 



^C2f» (3- 
CLASS* XX( 



Entered according to Act of Congress, in the year 1907, by 

LEA BROTHERS & CO. 

in the Office of the Librarian of Congress. All rights reserved. 



THIS BOOK 



IS 



DEDICATED TO MY FRIEND AND COLLEAGUE 

J. CHALMERS Da COSTA, M.D. 

PROFESSOR OF THE PRINCIPLES OF SURGERY AND CLINICAL SURGERY IN 
THE JEFFERSON MEDICAL COLLEGE OF PHILADELPHIA. 



PREFACE TO SIXTH EDITION 



When the physician is at the bedside, or in his consulting room, 
he develops the diagnosis of the ailment of his patient by an analysis 
of the symptoms of which he hears, which he sees, and which be 
discovers on making a thorough physical examination of the organs 
of the body. Lastly, he calls to his aid the methods of examination 
which are carried out in the laboratory. 

At the present day there Is a great tendency on the part of prac- 
titioners who can command laboratory assistance to ignore the 
measures which had to be relied upon before laboratories were 
developed, with the result that the various methods of physical 
diagnosis involving refinement in the senses of touch and hearing 
and in observation are in danger of becoming lost arts. On the 
other hand, practitioners who do not live near well-equipped 
laboratories, or do not possess them, are sometimes careless in 
the matter of resorting to methods of laboratory investigation. 

This book is designed to deal chiefly with the diagnosis of disease 
by means of the symptoms presented by the patient, and takes up 
laboratory methods only in those cases in which they are essential 
to arriving at correct results, as, for example, in the examination 
of the blood and urine. In other words, the object of this volume 
is to place before the physician and student the subject of medi- 
cal diagnosis as it is met at the bedside. To accomplish this the 
symptoms used in diagnosis are discussed first, and their applica- 
tion to determine the character of the disease follows. Thus, in- 
stead of describing locomotor ataxia or myelitis, there will be found 
in the chapter on the Feet and Legs a discussion of the various 
forms of and causes of paraplegia, so that a physician who is con- 
sulted by a paraplegic patient can in a few moments find the various 
causes of this condition and the differential diagnosis between each. 
So, too, in the chapter on the Tongue, its appearance in disease, 
both local and remote, is discussed. In other words, this book is 
written upon the only plan which can be followed in practice, 
namely, the upbuilding of a diagnosis by grouping the symptoms. 



viii PREFACE TO' SIXTH EDITION 

In the ordinary treatises the reverse of this plan is followed, com- 
pelling the physician to make a supposititious diagnosis and then 
to turn to his reference book and compare the article dealing with 
the supposed disease, when if the description fails to coincide with 
the symptoms of his case he must make another guess and read 
another article. In this book, however, the discovery of any marked 
symptom will lead directly to the diagnosis. Thus, if the patient is 
vomiting, in the chapter on Vomiting will be found its various causes 
and its diagnostic significance, and the differentiation of each form 
of this affection from another. The present edition contains a large 
number of illustrations taken from actual cases. 

Basing his efforts upon the experience which he has had in both 
didactic and clinical teaching of large classes of students during the 
last twenty-three years, the author hopes that the work may in some 
degree lighten the labors of the general practitioner and student. 

The author wishes to express his appreciation of the cordial 
reception given to this work in its earlier editions, and to bespeak 
for it an equally favorable acceptance in its present form, the 
more so as it appears simultaneously with the twelfth edition of 
his Text-book of Practical Therapeutics, to which it has always 
been a companion volume. 

H. A. H. 

N. W. Cor. Spruce and Eighteenth Sts., 
Philadelphia, 1907. 



CONTEXTS 



INTKODUCTION. 

GENERAL DIAGNOSTIC CONSIDERATIONS. 



CHAPTER I. 

THE FACE AXD HEAD. 



PAGE 



The expression and color of the face — Facial deformity — Facial paralysis, 
unilateral and bilateral — Ptosis — Facial spasm — The shape of the 
head — The movements and position of the head and neck ... 9 



CHAPTER II. 

THE HANDS AXD ARMS. 



The general appearance of the hands and arms — The shape of the hands 
in disease — Spasms of the fingers — Tremors of the hands — Paralysis 
of the hands and arms .... 34 



CHAPTER III. 

THE FEET AXD LEGS. 

The general appearance of the feet and legs when clothed — The gait — 
Spastic paraplegia — Paraplegia without spastic contraction — Crural 
monoplegia — Deformities of the feet and legs — The joints — Altera- 
tions in the nutrition of the feet and legs aside from a change in the 
muscles 59 



CHAPTER IV. 

HEMIPLEGIA 99 



CONTENTS 
CHAPTER V. 

THE TONGUE, MOUTH, PHARYNX, AND ESOPHAGUS. 



PAGE 



The general appearance of the tongue — Its coating — Its appearance 
in poisoning — Fissures and ulcers of the tongue — Eruptions on the 
tongue — Atrophy and hypertrophy of the tongue — Paralysis — Tremor 
and spasm of the tongue — Tonsillitis — Diphtheria — Pharyngitis — 
Disease of the esophagus 112 

CHAPTER VI. 

THE SKIN. 

The color of the skin — Eruptions on the skin — Gangrene, ulcers, and 
sloughs — Scars, sweating, dryness, edema, hardness — Anesthesia 
and hemianesthesia — Paresthesia, hyperesthesia, itching . . . .129 

CHAPTER VII. 

THE THORAX AND ITS VISCERA. 

The inspection of the normal and abnormal chest — Their topography — 
Alterations in the shape of the thorax — The rhythm of the respira- 
tions — The results of using inspection, palpation, percussion, and 
auscultation in health and disease — The characteristic signs and 
symptoms of the various diseases of the thoracic organs . . . .191 

CHAPTER VIII. 

THE PULSE AND BLOODVESSELS. 

Feeling and counting the pulse — The condition of the bloodvessels on pal- 
pation — The quality, force, tension and volume of the pulse in health 
and disease 265 



CHAPTER IX. 

THE ABDOMEN AND THE ABDOMINAL VISCERA. 

The surface of the abdomen — Changes in the appearance and shape of 
the abdominal wall — The signs and symptoms of disease of the 
abdominal organs 279 

CHAPTER X. 

THE BOWELS AND FECES. 

Constipation and diarrhea — The cause of these two symptoms and their 
diagnosis — The diseases in which these symptoms occur — Choleraic 
diarrhea — Dysentery — The color of the feces — Intestinal parasites . 314 



CONTENTS xi 

CHAPTER XI. 

THE URINARY BLADDER AND THE URINE. 

PAGE 

Disorders and diseases of the urinary bladder — Retention of urine — 
Incontinence of urine — The characteristics of normal and abnormal 
urine — The normal and abnormal contents of the urine— Their 
significance — Tests for the contents of the urine 329 



CHAPTER XII 

THE BLOOD. 

The various forms of red and white corpuscles— Their proportionate 
number in health and disease Alterations in their form and char- 
acter — The hemoglobin of the blood in health and disease — The 
various forms of anemia — Leukemia and pseudoleukemia— Para-: 
of the blood — The blood in typhoid fever and diabetes .... 375 



CHAPTER XIII. 

THE EVE 

The general diagnostic indications afforded by the eve — Diplopia and dis- 
order of the external ocular muscles — Strabismus and squint — Dis- 
order of the internal ocular muscles — The pupil — Hemianopsia — The 
visual fields — Color vision — The optic nerve and its lesions — Retinitis 
— Amblyopia and blindness 411 



CHAPTER XIV. 

CHILLS, FEVER, AXD SUBNORMAL TEMPERATURE-. 

Chills — The methods of taking the temperature — The significance of 

fever — The febrile movements of various diseases 442 

CHAPTER XV. 

HEADACHE AXD VERTIGO. 

The causes of headache — Digestive headache — Headaches due to the 
eyes — Headaches due to cerebral growths and abscess — Headaches 
due to syphilis — Headaches complicating acute diseases .... 46S 



CHAPTER XVI. 

COMA OR UXCOXSCIOUSNESS 4S4 



xii CONTENTS 

CHAPTER XVII. 

CONVULSIONS OR GENERAL SPASMS. 

PAGE 

Definition of a convulsion — The convulsions of epilepsy in its various 
forms — Of infancy — Of lwsteria — Tetanic convulsions — Tetany — 
Spasms — Chorea 491 

CHAPTER XVIII. 

HICCOUGH, VOMITING, REGURGITATION, AND THE CHARACTER OF THE VOMIT. 

Due to uremia — Cerebral lesions — Intestinal obstruction — Peritonitis — 
Cholera — Gastric disease — Hepatic disease — Poisons — The appearance 
of vomit 508 

CHAPTER XIX. 

COUGH AND EXPECTORATION. 

The varieties of and diagnostic significance of cough — The causes of 

cough — The sputum — Its pathological significance 525 

CHAPTER XX. 

PAIN. 

The kinds of pain — The significance of its locality — Colic 536 

CHAPTER XXL 

TENDON REFLEXES AND MUSCLE TONE. 

The knee-jerk and ankle clonus — The arm-jerk — The significance of 

decreased and increased reflexes 552 

CHAPTER XXII. 

SPEECH. 

The changes in the speech and voice — Their significance — Aphasia — 

Apraxia — Alexia — Paraphasia . 557 



PRACTICAL DIAGNOSIS 



INTRODUCTION. 

GENERAL DIAGNOSTIC CONSIDERATIONS. 

A clear understanding by the physician of the value of the symp- 
toms of disease which he sees and of those described by the patient 
is of vital importance for the purpose of diagnosis and treatment, 
and one of the advantages of older physicians over their younger 
brethren is the ability which they have gained through long training 
to grasp the essential details of a case almost at their first glance at 
the patient. Much of this ability is unconsciously possessed because 
it is gained by a gradual process, yet it is none the less valuable, and 
its possession often impresses the patient with the insight which his 
physician has into his case. At first it is impossible for the novice 
to cast aside the minor symptoms, which the patient emphasizes as 
his major ones, and to perceive clearly that one or two facts that 
have been belittled in the narration of the story of the illness are in 
reality the stalk about which everything else in the case must be 
made to cluster. 

While the physician should train his eye to take note of all varia- 
tions from the normal which are shown by the patient, he must be 
careful not to permit himself to depend for his diagnosis on these 
signs alone nor upon those described by the sick man. On the con- 
trary, he should carefully train his senses of touch, hearing, sight, 
and discover the so-called physical signs which can be elicited only 
by auscultation, percussion, palpation, and mensuration. The 
objective symptoms seen by the physician, the subjective symptoms 
described by the patient, and the so-called physical signs elicited by 
the methods just named, are to be joined together in forming a diag- 
nostic view of the case. Unless this combination is made, a faulty 
diagnosis will often be reached. In many instances chemical and 
microscopic examinations of the blood, the urine, the feces, and even 
of the tissues themselves, may be needful to determine in a given 
case what the ailment may be. 

Again, it is never to be forgotten that negative signs are as impor- 
tant as positive signs in many cases. The absence of a heart mur- 
1 



2 INTRODUCTION 

mur in a case of failing circulation is not a sign that the heart valves 
are healthy, but that the heart is too feeble to make a murmur, and 
the absence of rales or clearly heard breath sounds in a lung may be 
due to engorgement without exudate instead of indicating that the 
lung is not diseased. 

The Art of Observing the Patient. — Let us suppose the patient 
before the physician is one who has been able to walk into the 
office or dispensary. The attentive physician can at once gather 
much information about the case from the clothing, the gait, the 
build, the voice, the expression, and the manner. The thin man, 
with a peaked face and provided with an unusually warm overcoat, 
and still further wrapped up with a muffler almost to his eyes, is in 
all probability a sufferer from some pulmonary or throat difficulty, 
while the heavily built, phlegmatic individual, with a large head 
and well-filled paunch, is much more apt to suffer from gastro- 
intestinal or biliary catarrhs. Such a person will probably be one 
who habitually wears his coat open on the coldest days. Again, 
chronic drunkards, or persons whose mental powers are failing, 
often are exceedingly careless about their clothing, buttoning the coat 
or the trousers with the wrong buttons, and keeping the garments 
dirty and spotted. Some cases of diabetes have first been discov- 
ered by the white spots on the trousers, as the result of the patient 
having allowed a few drops of urine to fall on the cloth, where 
they have dried. Old men who have incontinence of urine often 
wear trousers which are stained in front, and they often have an 
ammoniacal odor about them from this cause. 

The various forms of gait which indicate actual disease will be 
found discussed in the chapter on the legs and feet, but it may be 
mentioned in passing that, in addition to these changes, which are 
dependent upon actual disease of the legs or the nervous system 
supplying them, the bearing and stride of a patient will often give 
a clear idea of his general tone. The neurasthenic patient walks 
feebly or with a step that might be called ataxic, while the strong, 
hearty man of good physique strides along with a gait quite 
different from this, or from that of an individual who is delicate 
and feeble. 

Similarly, the patient's build betokens disease or health. The 
thin, tall, and hollow-chested person is recognized as a fair mark 
for the tubercle bacillus, and the heavy, closely knit, phlegmatic man 
as one who may suffer from hepatic or circulatory disorders. Again, 
the bearing of a person possessing a highly organized nervous system 
shows itself in the constant activity of his mind and body. No part 
is quiet for more than a moment, and drugs are more apt to produce 
extraordinary symptoms as the result of idiosyncrasies in this type 
of patient than in any other. 



GENERAL DIAGNOSTIC CONSIDERATIONS ,'j 

The breath of the patient may call the physician's attention to 
some important facts in connection with the case. If it is sweet 
or vinous in odor, this may be due to diabetes mellitus; or if it be 
ammoniacal or urinous, uremia may be present. The previous use 
of bismuth may give it a garlic-like smell, due to the contaminating 
tellurium and various aromatic or volatile drugs, such as turpentine 
or copaiba, may be eliminated in the breath. In cases of advanced 
bronchiectasis the breath is often foul, and is insupportably so in 
gangrene of the lung or when an empyema has ruptured into a 
bronchus. It is similarly offensive in gangrenous stomatitis, and 
often very disagreeable in tonsillitis. In diphtheria it has a peculi- 
arly sickening and sweetish odor. When the odor is not dependent 
on these causes it may be due to ozena, or chronic atrophic nasal 
catarrh, to the presence of decaying food between the teeth or secre- 
tions in the crypts of the tonsils. Moderate fetor is usually due to 
disordered digestion and constipation. 

When the physician has gathered as much information as possible 
as to the age and general condition of his patient, by a careful 
scrutiny of his face and extremities, of which scrutiny, however, the 
patient should be unconscious, he should ask him to tell what brings 
him for advice, and, as a rule, this will be the opportunity the sufferer 
seeks to pour out the story of his ailment as he sees or feels it. Often 
the story will seem wearisome, and, to the educated mind of the 
physician, wandering or unnecessary; but to the patient everv word 
seems of the greatest importance, and to show any lack of interest 
may give the impression of carelessness, or it may interrupt the story 
just as a most important symptom is about to be described. Even 
if the patient is unable to convey in words a very clear idea of his 
condition, the manner in which his story is told, the character of 
his speech, and the expression of his face while speaking may give 
useful information as to his ailment or general state. 

If, instead of the patient being an office or dispensary case, he is 
one who is being visited at home, the fact that the patient meets 
the physician in one of the living-rooms rather than in a bed -room 
indicates either that there is little immediate danger in the case, or, 
at least, that the difficulty is not acute, but chronic in type, as some 
slowly progressing form of pulmonary, cardiac, or renal disease. 
Of course, there are exceptions to this rule, as in the case of a patient 
who, having caught a heavy cold, is remaining indoors, but not in 
bed, for prudence' sake. Or, again, if on seeing the patient we find 
him sitting in a chair only partly dressed and propped up with pil- 
lows, or instead leaning forward upon the back of a chair placed in 
front of him, we know that he is the subject most probably of an acute 
or chronic heart disease, most likely an acute exacerbation of the 
latter. A glance at the face of such a patient, revealing a trembling 



4 INTRODUCTION 

nostril, blue lips, or an anxious facies, will aid still further in direct- 
ing attention to the heart or lungs, and the hands if examined will 
appear relaxed and livid or darkened in hue, indicating capillary 
stasis and deficient oxidation in the blood. In other cases, however, 
the patient found sitting propped up with pillows may be a con- 
valescent from some long illness; but if so, the general atmosphere 
of the patient is better, and the surroundings are apt to be more tidy. 

If we find the patient in bed, he may be lying abnormally quiet 
as the result of faintness or acute nausea, or, perhaps, from partial 
or complete coma due to cerebral or renal disease, or from the effects 
of some drug; or, again, he may be rolling about the bed from the 
pain of acute bellyache, or be keeping his legs and body very still 
while his hands and head are ever on the move to prevent anything 
from suddenly approaching or touching his abdominal wall, as in 
peritonitis. The striking difference between the activity of the 
head and the fixation of the lower part of the body, in peritonitis, is 
notable. Sometimes, however, anxious restlessness indicates acute 
internal or external hemorrhage ; but here the movements are minute 
though active, and the patient does not expend so much strength as he 
does when suffering from pain. 

In acute articular rheumatism the patient lies, if many of his 
joints are involved, in a peculiarly helpless position, as if he were 
glued fast to the bed, although the active movement of the eyeballs 
as they follow persons moving about the room gives quite a different 
aspect from that of a patient immovable from stupor. 

Usually a patient who is lying on his side turns on his back 
as the physician or nurse approaches, in order to face his visitor; 
but if he persistently remain on the side without moving, except partly 
to turn his head, we may suspect that in that posture he is most com- 
fortable, and that the position is assumed for its comfort or to relieve 
pain or dyspnea, which are suffered from when another attitude is 
taken. Thus, in acute pleurisy the patient lies with the affected side 
uppermost, because it is too sore to permit him to touch it to the bed ; 
whereas if the stage of effusion has arrived, he lies on the affected 
side, in order to give the side which is healthy free play in compen- 
satory respiratory movements, and to remove the pressure of the 
effusion from the healthy lung. If the patient lying in this posture 
is not suffering from pleurisy, his position may be due to an effort 
to relieve the discomfort caused by an enlarged liver. The fact 
that the patient lies constantly on the back is also a characteristic 
of grave and advanced disease in some instances. Very ill persons 
almost never lie on the side, and the fact that a desperately ill 
patient of yesterday is found lying on the side today is encouraging. 

Persons with severe heart disease, emphysema, or chronic bronchi- 
tis are rarely, if ever, able to lie prone in bed, and have to be more or 



GENERAL DIAGNOSTIC CONSIDERATIONS 5 

loss propped up with bed-rests and pillows. Large growths in the 
abdominal cavity producing pressure on the diaphragm also necessi- 
tate this semiprone posture, and double pleural effusions, or pul- 
monary consolidation or edema, require the upright or half-reclining 
attitude in order that the upper parts of the lung may be used to 
advantage. 

In asthma the patient frequently is found sitting up in bed with 
the arms reaching back of the hips as props to fix the chest and to 
hold the body erect. So too in advanced cardiac and renal disease 
the patient will often take a seat in a chair and rot the head and 
hands on the back of another chair placed in front of him, both 
eating and sleeping in this attitude. 

Again, if the patient wakes when spoken to and then drops off to 
sleep at once, some form of poisoning may be present, as from opium, 
or the poisoning of advanced hepatic or renal disease may be 
present. 

(For the significance of picking at the bedclothes, see chapter 
on the Hands and Arms.) 

The Art of Questioning the Patient. — We can next pass to a consid- 
eration of the objects to be sought in questioning a patient as to the 
illness from which he is suffering. Often much information can 
be gained by a well-directed question, and a favorable impression 
can be made upon the patient by the manner in which it is put 
and the bearing which it has on his case. Thus, if a man is 
evidently much emaciated and his clothes fit him loosely, a question 
in regard to his loss of flesh is very appropriate; but if he is mani- 
festly too stout for comfort such a question will be most unwise. 
Or, again, if a young married woman comes complaining of 
constant sickness of the stomach and a fanciful appetite, and 
the physician directs all his questions to the condition of the 
stomach without an eye to a slight increase in size about the 
waist or below it, his professional acumen is in grave danger of 
being libelled by that same woman, who knows, or soon finds out, 
that her discomfort is due to pregnancy. 

If the woman is unmarried and there is no evidence of gastric 
disorder on her tongue, it is well to remember what Battev, of 
Georgia, said in regard to this condition: "Always believe a voung 
unmarried woman with abdominal tumor, of high social position 
and unimpeachable virtue, if she has been watched over by a pla- 
tonic and abstemious young cousin of the male persuasion while 
the mother w T ent out, to be pregnant." 

Again, if a married woman of some years tells her physician 
that she has no children, the physician naturally asks some ques- 
tions which elicit the fact that she has had frequent miscarriages. 
He in this way finds out quite as much about probable syphilitic 



6 INTRODUCTION 

infection as if the question had been put: "Have you ever had a sore 
on your privates?" which would embarrass the patient, produce 
domestic troubles, and probably be lied about if her husband is 
forced to answer the question. 

Again, when asking a woman about the health of the living 
parents, or the cause of death of the dead, care should be taken 
not to ask a direct question, as, for example, whether the mother 
has died of cancer, for the patient may be already greatly worried 
lest she has that disease. It is better to ask the cause of death, or 
of the illness she is suffering from. If the story is that the parents 
died of "bronchitis," the real cause of death was probably tubercu- 
losis of the lungs. 

If the patient complains of pain, past or present, the best way 
in which to discover its true seat is to ask him to place his hand on 
the affected part, as in this way errors in his description of his 
anatomy will not be committed, and false impressions will not be 
conveyed to the physician's mind. Even this direct method of 
showing the area of pain is not to be absolutely relied upon, for 
often pains are referred to parts in which there is no disease. Thus, 
the pain of coxalgia is apt to be felt in the knee and ankle, and in 
children the pain of pulmonary or cardiac disease is often described 
by the patient as felt in the abdomen. If the pain has been really 
abdominal, there will, in many cases, have been diarrhea or free 
passage of flatus. It is not to be forgotten, on the other hand, that 
a question which discovers the fact of several movements of the 
bowels does not prove the presence of true diarrhea, because a 
purgative may have been taken by the patient. 

p*» In asking questions as to constipation the physician must not 
forget that the opinion of the patient as to what constitutes regu- 
larity of bowel movement is of very little value in many instances. 
A daily movement is not known to many patients, and a movement 
every few days may be quite sufficient to justify the statement, in 
their opinion, that no constipation is present. 

The young physician, in particular, in asking questions of women 
patients of the better class, should not hesitate to ask direct ques- 
tions as to the state of the bowels or of the menstrual function. To 
hesitate or ask indirect questions about such matters simply pro- 
duces embarrassment which otherwise would not exist, and intimates 
that the question is one of doubtful propriety, when in reality it is 
most important and proper. 

The Examination of Children. — If the patient to be examined is a 
child, it is well for the physician to remember that his presence as a 
stranger may be a source of alarm, and that the association in the 
child's mind of sickness and the doctor, and badly tasting medi- 
cines, is sufficient to render him a much-to-be-dreaded individual. 



GENERAL DIAGNOSTIC CONSIDERATIONS 7 

Generally it is best, on entering the room where the child is, to 
pretend to pay no attention to it whatever, but to engage in con- 
versation with the mother or other person, speaking of the case in 
a way which the child will not understand. Very often this very 
lack of attention will result in the child forcing the recognition 
of his presence upon the physician by making the first advances 
toward friendship, and this is particularly apt to be the case if the 
child is already spoiled by over-attention by the family and friends. 
Time should always be given the child to grow accustomed to the 
peculiarities of the visitor, and if any instrument for diagnosis is 
to be employed it is best to hold it in the hand as if it were a play- 
thing before attempting to put it into actual use. The tact which 
the physician must exercise in diverting a sick child is an essen- 
tial to the successful treatment of children. Some physicians are 
welcomed to a house by the sick and well as Santa Claus would be, 
and others, devoid of the trait of amusing children, are fled from 
as if they w T ere dragons. 

During the time that the physician is allowing the child to get 
accustomed to his presence he should be gaining much useful infor- 
mation about the case by observing the movements and expressions 
of the child; its color, size, nutrition, breathing; the shape and size 
of its head; the condition of its lips, whether moist or dry, red, livid, 
or pale; and, if the child is speaking, the tone of its voice, or, if crying, 
the character of its cry. It is needless to state that a child may cry 
from fright, from pain, anger, or hunger. Constant screaming 
is, however, nearly always due to the pain of earache or hunger, 
for abdominal colic is usually intermittent. If there be pain in 
the ear, the hand will often be rubbed over the affected side of the 
head, and the child will not be pacified by the offer of the breast. If 
the child coughs, and then begins to cry, pneumonia or pleurisy 
may be present; or in other cases the pain is so great that the child 
is cryless. A sharp, piercing shriek indicates the pain of earache 
or of meningitis in many cases. 

If a crying child be placed at the breast, which it takes with 
avidity only to drop the nipple in a moment with a cry of pain or 
anger, one of several conditions is present: either the child has 
stomatitis or the breast is empty; or, again, if it seizes the breast 
and then lets go with a gasp, it may have coryza or syphilitic 
snuffles, which prevents it from breathing through the nose while 
sucking. Similar signs may be present in any other condition pro- 
ducing shortness of breath. 

If a child over four months of age cries and sheds no tears in 
the course of an illness, this is an unfavorable sign. 

It is important to notice whether there is languor or a tendency 
to play. A healthy infant, when awake and well fed, is always 



8 INTRODUCTION 

kicking and cooing and moving its arms about, and has a happy 
expression on its face; whereas if any cerebral trouble is present, 
it often has an anxious frown, or its hands are placed on the side of 
its head or rubbed over the vertex. 

In a perfectly healthy child which is sleeping, the respiration 
should be practically inaudible, and it is a good practice to note the 
regularity of the breathing in all patients while they are asleep, 
as it is then unaffected by voluntary effort. In children a sighing 
breathing, or one disturbed in rhythm, often indicates a disturbed 
digestion or fever. 

The physician should always, by careful questioning of the nurse 
or mother, find out how long the illness has lasted, the manner in 
which it began, the fact as to whether a similar attack has occurred 
before in this or other children of the family, and the state of the 
temper, appetite, bowels, and urine of the patient, for an irritable 
temper in a child means ill health, as does also a poor appetite, 
constipation, diarrhea, or abnormal urine. 

The expression of the face, shape of the head, and similar note- 
worthy points in the diagnosis of the case will be more thoroughly 
discussed in the chapter devoted to these parts. (See chapter on 
the Face.) 

When it comes to a close examination of the child, great care 
must be exercised. The character and rapidity of the respirations 
are best studied at a distance before excitement has disturbed them, 
and the best time for listening to a young child's chest is when it is 
held over the shoulder of the mother, as if she were carrying it for 
a walk, or, if the child can be taken in the physician's arms, its 
buttocks should rest on one hand, while the front of its chest rests 
against the other. In this way the physician can listen to the back 
of the chest without difficulty, keeping the child amused by 
walking up and down the room while it is in his hands. 

If it is not possible by any bribe to cause the child to protrude 
the tongue for examination, the physician will often be able to see 
this organ when the mouth is widely opened in crying. 

In taking a child's pulse it is best to take it while it is asleep, if 
possible, as the excitement of the physician's visit or the crying on 
awakening will greatly increase the pulse rate. 



CHAPTER I. 

THE FACE AND HEAD. 

The expression and color of the face — Facial deformity — Facial paralysis, 
unilateral and bilateral —Ptosis — Facial spasm The shape of the hea 1 - 

The movements and position of the head and neck. 

So much can be learned by the physician from the expression and 
general appearance of a patient's face and the carriage and shape of 
his head that a careful inspection of these parts should always be 
made. For this reason, in the consulting-room and at the bedside, 
the physician should always arrange his chair in such a way that 
the light falls upon the face of his patient, while his own is in the 
shadow, and this is of importance not only because the facial expres- 
sion of the patient can thus he well seen, hut also because it prevent^ 
the patient from making a too close scrutiny of the physician's 
face with the object of detecting encouragement, lack of sympathy, 
or alarm. 

THE FACE. 

The Expression. — The expression is produced by the formation of 
creases, or alterations in the contour of the skin and subcutaneous 
tissues by trophic and muscular action, and these changes are in 
time brought about and perhaps made permanent by the mental 
tendencies and habits of the patient, his temperament, his intel- 
lectual development, his exposure to outdoor or indoor influences, 
and, finally, and these are very important, by pathological processes 
which may be going on somewhere in his body. The temper of 
the man also affects his expression, particularly as he approaches 
middle life, and he looks amiable, capable of sudden anger, or sullen, 
as the case may be. 

The intellectual face is easily recognized. Sometimes it is deeply 
thoughtful and placid, at others eager or keenly alive to the sur- 
roundings or the conversation, and it separates the man descended 
from several generations of men who have lived as thinkers from him 
whose ancestors have been but recently wage-earners by physical 
labor, involving only ordinary human intelligence. 

The skin of the face and the expression about the eyes of one 
who has been exposed for years to the weather are so characteristic 



10 THE FACE AND HEAD 

as to need no description, while the face of the clerk, whose life is 
almost entirely spent indoors, is pale and wan. 

Fulness of the lips, particularly of the lower lip, is supposed to 
be present in persons of strong sexual appetite, and often indicates 
a phlegmatic temperament, whereas the thin, mobile lip is typical 
of the high-strung, nervous individual. 

The expression of the lips as a whole is also to be regarded in 
connection with the expression of smiling. The risus sardonicus 
of strychnine poisoning or tetanus is quite characteristic, and the 
simple smile of hysteria is equally notorious. 

Similarly, the face of a person who uses alcohol to excess is 
generally flushed, heavy, and more or less expressionless. The 
eyelids are redder than normal, and the skin is apt to be puffy and 
unhealthy looking. Women at the menstrual period, or when suf- 
fering from menstrual disorders, often have dark areas under the 
eyes, and pigmentation of the eyelids is often seen very early in 
pregnancy. In women, and sometimes in men, excessive fatigue 
and loss of sleep cause marked infra-orbital discoloration. A 
puffiness under the eyes, most noticeable in the morning, may indi- 
cate renal lesions or the excessive use of arsenic; or if it is unilateral 
it probably depends upon some local inflammation of the eye or 
rarely upon disease of one of the cephalic sinuses. So, too, an 
ecchymotic spot under the eye may be due to a bruise, to some one 
of the forms of purpura, or to scurvy. 

The color of the face is discussed in the chapter on the Skin, but 
it is not out of place to note at this point the pallor of the face in 
fright, faintness from hemorrhage (acute or chronic), that due to 
lack of proper food, and the peculiar pallor of chlorosis. In the 
latter disease the faint yellowish-green tinge of the skin in some parts 
of the face, which still retains its plumpness, is quite typical. A 
parchment-like skin stretched over the face so that it appears as if 
stretched and dried over the under structures is seen in some young 
persons suffering from syphilis, and in some cases of hepatic 
cirrhosis. 

The color of the face may be rendered gray or bluish by the 
ingestion of overdoses of the coal-tar products, such as acetanilid, 
antipyrine, and phenacetin, and it is curious that this effect is best 
seen when the patient is viewed at a little distance. 

(For the significance of facial cyanosis, see chapter on the Skin.) 

In view of the extraordinary variations seen in the expression of 
the face in the healthy it is not surprising that this part of the body 
should give the physician, when studying disease, so much useful 
information. It is an interesting fact, too, and one not unworthy 
of note, that the true facial expression of a disease is rarely aped by 
a malingerer, and in all diseases is unrecognized by the patient even 






THE FACE 11 

though he sees himself several times daily in a looking-glass. Thus 
it is by no means uncommon to see a person who is suffering from 
the onset of some sudden and grave disease bearing upon his face 
what we call "an expression of anxiety," when he himself as yet 
has no conception of the gravity of his illness. This expression is 
very characteristic of serious illness, and, though difficult to describe, 
when recognized becomes quite valuable as a diagnostic factor, 
particularly as it rarely, if ever, is exaggerated by the patient who 
bears it. It is seen most markedly in cases of severe acute croupous 
pneumonia or in peritonitis, or after severe injuries. 

When persons have had continuous pain for a long time, as in 
patients who have growths of a malignant character or other organic 
disease, the expression of the face, naturally gentle, often becomes 
hard and stony, or if the pain be in the head, the expression is not only 
that of pain, but of profound mental depression. In cases of \ isceral 
carcinoma the face becomes thin, its skin yellow and straw-colored, 
and oftentimes greasy and thick, and there is often a marked 
expression of anxiety. On the other hand, the patient sometimes 
has a dogged expression on his face as if he had been told of the 
true cause of his illness, and was rebelling against the inevitable 
progress of the disease. 

In the case of children, much information can be gained as to the 
state of the system by the facial expression, particularly while the 
child sleeps. If it is asleep and healthy and well, the eyelids are 
closed, the lips are never so slightly parted, the nostrils are practically 
immobile, and the general expression is very peaceful. If, on the 
other hand, the eyelids of a sleeping child are slightly parted so as 
to show the whites of the eyes, there is probably present some diges- 
tive or nervous disturbance, perhaps accompanied by moderate 
pain. If in the course of an illness the eyelids remain far enough 
apart to result in glazing of the conjunctiva from dryness, this is a 
sign of grave import. Again, twitching of the eyelids often indi- 
cates nervous irritation or the early stages of the convulsive state, 
and it is not uncommon for an expression to pass over the face of 
a child who, while sleeping, is suffering from pain, which begins as 
a smile and ends with a dra wing-in of the corners of the mouth, an 
expression somewhat like that seen on the face of a waking child 
when it seems to be in doubt as to whether to laugh or to cry. 
Whether asleep or awake a child in pain, if not crying, has a pinched 
look about its nose and mouth, and sometimes some idea of the 
seat of the pain may be gained by the part of the face which is drawn. 
When pain is in the head, the forehead is apt to be wrinkled into a 
frown; if the nose is pinched and drawn, it is said to show that the 
pain is in the chest; and if the upper lip is raised, pain is probably 
felt in the belly. 



12 THE FACE AND HEAD 

Aside from these symptomatic manifestations, however, we find 
in the face of a child several evidences of important diathetic ten- 
dencies, or even hereditary diseases. Thus we see the light flaxen- 
haired, slimly built child with a refined, spirituelle face and trans- 
parent skin, whose temporal veins can be easily traced and whose 
expression is often thoughtful and deep. Such a child often comes 
of tuberculous parents, and is frequently a victim of tuberculosis, in 
one of its rapid forms, as it approaches puberty. Or, again, the 
child is "stocky" and cheesy looking, apparently solid and sturdy, 
but its features are heavy or perhaps even coarse, while its neck is 
thick and short. Such a child is often a victim of tuberculous 
bone or lymphatic disease. In other instances a square projecting 
forehead with faulty bone development elsewhere indicates rickets, 
or an immense, bulging forehead with a wizened, puny face beneath 
shows hydrocephalic tendencies. Sometimes a broadness of the 
bridge of the nose or marked flatness of it indicates congenital 
syphilis. Such a child is often much wasted, its features pinched, 
and its lips thin, while the flattened nasal bridge is bluish, and its 
face is often that of a little old man, shrivelled and wrinkled. 
Mucous patches at the corners of the mouth or around the anus 
are often found in such cases, and, if found, confirm the diagnosis 
of infantile syphilis. Finally, in respect to facial expression in 
childhood, attention must be called to the "fish mouth," vacuous, 
and "nose-pinched" expression of those children who are "mouth- 
breathers" from nasal obstruction (Fig. 1). Great immobility of 
the lips and cheeks may be due to mucous patches or other ulcer- 
ations of the buccal mucous membrane; and if high fever is 
present, the presence of herpetic blisters about the lips points to 
the possible presence of croupous pneumonia in the child or adult. 

The face of a patient with acute fever is apt to be red and flushed, 
and the eyes bright; and if the disease be distinctly infectious, as in 
some cases of pneumonia, tuberculosis, and acute articular rheuma- 
tism, it may be covered with sweat. 

In adults the facial expression of many diseases is even more 
characteristic than it is in children. Thus, we see in acute pul- 
monary phthisis the widely opened eye, the hunted expression, the 
quivering nostrils, the red flush over the malar bones, the wasting 
and dryness of the hair and skin, and the eager or in other cases 
apathetic glance of the eye. 

In severe croupous pneumonia the flushed face, with a deeper red 
on one cheek than the other, the anxious expression, and the dilated 
nostril are noteworthy; and in the dyspnea of heart disease the 
dilated nostril and constant opening of the mouth, as if seeking for 
air, with the facial pallor or cyanosis, are characteristic. Often, 
too, in chronic cardiac or pulmonary disease producing slight diffi- 



THE FACE 



13 



culty in respiration, the patient's lips are seen to be slightly parted 
and dry, and may appear somewhat cyanotic. In children suffer- 
ing from lesions of the mitral valve of the heart it is very common 
for some blurring or indistinctness of the features to be present. 

One of the most characteristic facial expressions that we meet 
with is that of typhoid fever or fevers of a typhoid type. The face 
is dull and expressionless; the teeth are covered with sordes, which 
become brown and blackish by exposure or by discoloration from 
medicines and foods; the lips are often moved in a low muttering 
delirium; and the whole appearance is that of apathy. Even when 




p IG i_ — Mouth breather, from obstruction of the pharynx; open mouth; vacant expression; 
pinched nostrils; dull eyes; drooping eyelids; round shoulders. 



spoken to, the face of a patient suffering from enteric fever rarely 
lights up in response to the greeting. 

Equally, if not more, characteristic is the facial expression of 
acute peritonitis. The upper lip is drawn up in such a way as to 
show the teeth, and the expression of anxiety and nervous unrest 
is well developed. Similarly in abdominal pain due to other causes 
than peritonitis there is often a twitching of the muscles of the lip 
and about the eye which is quite typical. This twitch is said by 
Fothergill to be peculiar to pain below the diaphragm, and he is 



14 THE FACE AND HEAD 

also responsible for the statement that it is best seen in the face of 
the parturient woman in the second stage of labor. 

The facial expression of hysteria may be apathetic, or it is that 
of devotion, rage, or grief, and these expressions are fixed if the 
patient be cataleptic. If she is not cataleptic, not infrequently one 
expression may succeed the other, or in their place there. comes that 
curious smile or vacuous expression of the face which is so char- 
acteristic. It should be remembered, however, that this vacant 
fatuous look may occur in women suffering from the early stages of 
disseminated sclerosis and in children with chorea. Then we have 
the elated facial expression of general paralysis of the insane, the 
excited look of acute mania, the beaten, weary, careworn look or 
apathetic glance of nervous exhaustion, and the hopeless expression 
of melancholia. 

The face of paralysis agitans, sometimes called the " Parkinsonian 
visage," is distressed and pathetic, and yet somewhat intense. (See 
chapter on the Hands and Arms, that part on Tremor.) 

A pale, puffy face, generally looking worn and weary, may be seen 
in cases of chronic or subacute renal disease. In children there is 
often in this condition a peculiar transparent or pearly look in the 
lower eyelid, so that it seems somewhat pellucid. Great swelling 
or edema of the face is seen in erysipelas, dropsy (Fig. 2), and simple 
inflammatory swelling. (See chapter on the Skin.) In trichiniasis 
the eyelids are often swollen early in the disease, and then recover 
their normal appearance only to become swollen again later in the 
malady. 

The facies of exhausting disease about to produce death is very 
characteristic, and is seen frequently in cholera and in tuberculosis 
of the lungs or any state associated with profound collapse, such as 
internal hemorrhage. It is accompanied by pallor, cold extremities, 
and difficult breathing. This is called the "Hippocratic face," 
and is peculiar in the sinking-in of the temples where the jaw muscles 
are inserted; the eyes are sunken, and around them are great 
hollows, so that the infra- and supra-orbital ridges become greatly 
accentuated. The eyelids are slightly parted, the cornea somewhat 
glazed; the nose pinched, its skin drawn; and the lower jaw some- 
what dropped. Such a facial expression, if typical, is a sure fore- 
runner of dissolution. 

When the face bears a sleepy, listless expression, the forehead 
being devoid of wrinkles, and there are present faulty movements 
of the lips, which cannot be approximated, as in whistling, and at 
the same time the patient is unable to close the eyes entirely, although 
the lids droop, the physician should think of the possibility of these 
being the early symptoms of what has been called the " f aciohumero- 
scapular" type of muscular atrophy. (Landouzy and Dejerine.) The 



77/ a; face 



15 



disease, as its name implies, speedily involves the scapulae and arms 
after affecting the face, and exophthalmos is often present. This 
form of muscular atrophy lacks the fibrillary twitchings seen in 
spinal progressive muscular atrophy, and there are no changes in 
electrical excitability, except that owing to the loss of muscle fiber 
the reaction is feeble. The facts that more than one member of the 
family is affected and that the disease is of long duration, added to 
these signs, render the diagnosis easy. It is a rare disease. 

An appearance of the face almost identical with that just described 
is seen in Friedreich's ataxia, and is often one of the earlier mani- 
festations of the disease; but the presence in Friedreich's ataxia of 





Fig. 2. — Face of a patient with general anasarca due to chronic parenchymatous nephritis. 
(From a patient in the author's wards, Jefferson Medical College Hospital.) 

the ataxic gait, the jerky articulation, nystagmus, loss of knee-jerks, 
and absence of muscular atrophy separate it from the Landouzy- 
Dejerine type of muscular atrophy just described as faciohumero- 
scapular atrophy. (See Ataxia in chapter on the Feet and Legs.) 
The facial expression of cretinism is exceedingly characteristic. 
The nose is broad and flat, the eyelids are swollen, the lips greatly 
thickened, and the enlarged tongue lolls out of the mouth, from 
which saliva constantly dribbles, while the waxy skin and subnor- 
mal temperature of the body, w T ith a poor circulation, slow respira- 
tion, and mental hebetude, complete the symptom group. There 



16 



THE FACE AND HEAD 



is nearly always in well-developed cases marked lumbar lordosis 
(Fig. 3). 

The facial expression of myxedema is heavy and listless, as a 
rule. (See chapter on the Skin.) 

In certain forms of leprosy the face often becomes leonine, or 
lion-like in appearance. 

Facial Deformity. — Facial asymmetry is sometimes seen as a 
congenital defect, and curiously enough is often developed in children 
who suffer from congenital wryneck. This is not to be confused 
with that extraordinary affection called facial hemiatrophy, which 




Fig. 3. — A cretin. (Dercura.) 

usually begins in childhood in one spot, and slowly proceeds until 
one side of the face, sharply outlined from the other, becomes wasted 
in its skin, muscles, bones, color, and hair. Even the eye may be 
sunken and shrunken. Rarely this wasting extends over the whole 
of one side of the body, and still more rarely is bilateral. 

Sometimes in facial hemiatrophy the wasting is accompanied by 
painful twitchings, which increase with mental excitement. More 
rarely there is decrease in the acuity of taste and hearing on the 
affected side, while myosis, sweating, or excessive dryness of the 



77/ A' FACE 



17 



skin may also be found on this side. Such symptoms as the last 
show involvement of the sympathetic nerve fibers. The changes 
are probably due to disease of the fifth (trifacial) nerve. 

As to whether circumscribed scleroderma (morphea) and facial 
hemiatrophy are identical — that is, whether the first is a well-devel- 
oped form of the latter — is not decided. Hyde apparently regards 
them as identical. (See chapter on the Skin, Scleroderma.) 




Fig. 4. — Acromegaly, showing the large face and hands. (Dercum.) 



Even more rare than facial hemiatrophy is facial hemihyper- 
trophy, one side remaining normal in size and the other becoming 
gigantic. 

The massive face of a person suffering from acromegaly is very 
characteristic (Fig. 4). The face has a full-moon broadness in 
myxedema. The enlargement of the bony parts of the skeleton, 
the kyphosis, and the comparative muscular feebleness of acro- 
megaly aid in the diagnosis of that disease, for in myxedema there is 
no true bony enlargement. The face in osteitis deformans is shaped 
like a triangle with the base upward, and the shafts of the long 
3 



18 THE FACE AND HEAD 

bones become weakened, and their surfaces roughened from periosteal 
deposits. (See chapter on the Hands and Arms.) 

Unilateral Facial Paralysis. — Very notable changes in the face are 
produced by paralysis, the palsy being, as a rule, unilateral and 
depending upon central or peripheral nerve lesions for its cause. 
Smiling, when unilateral paralysis is present, results in the drawing 
back of only one corner of the mouth (on the well side), and whist- 
ling or the pronunciation of labial sounds is difficult or impossible. 
The cheek of the paralyzed side is often puffed out with each expi- 
ration, but the wrinkling of the skin is on the side of the face which 
is not paralyzed, owing to contraction of the muscles which are 
unopposed. 

(For a description of the general anatomy and physiology of the 
nervous tracts involved in paralysis of the face and elsewhere, see 
chapter on Hemiplegia.) 

Unilateral paralysis is, as already stated, the form of facial par- 
alysis most commonly seen, and is generally due to injury of the 
facial nerve trunk. The lesion producing the paralysis may, however, 
be peripheral — that is, in the nerve itself — or central, that is, in the 
pons or the cerebral cortex. The former variety is the most common, 
provided the paralysis is purely facial, and it is usually due to in- 
flammation of the nerve sheath as it passes through the stylomastoid 
foramen, the loss of function being due to pressure on the axis 
cylinders owing to the presence of swelling in so limited a canal. 
Such an attack will generally be found associated with a history of 
exposure to cold or injury by a blow, or with that of middle-ear 
disease with caries of the petrous portion of the temporal bone follow- 
ing otitis, which inflammatory process causes pressure on the nerve. 
It is not necessary for the otitis to be suppurative or for caries to 
exist in all cases, for it seems probable that by the extension of inflam- 
mation along the chorda tympani such a paralysis may result. If the 
disease be in the petrous portion of the temporal bone, in addition 
to paralysis of the muscles of expression there will also be loss of 
taste in the anterior part of the tongue due to involvement of the 
chorda tympani. The mouth is dry, owing to a lack of saliva, the 
salivary gland being paralyzed, and there may be deafness from 
paralysis of the stapedius muscle. Still more rarely facial paralysis 
results from swelling of the parotid gland or from a tumor in its 
neighborhood, and it may occur as the result of pressure by growths 
at the base of the brain, syphilitic or otherwise, from fracture of the 
base of the skull involving the petrous portion of the temporal bone, 
and very rarely, when the disease occurs in the newborn, from hemor- 
rhage from the cerebellum during birth, or from pressure of forceps. 
(See below.) Finally, paralysis due to a peripheral lesion of the 
nerve may result from neuritis, and from primary hemorrhage into 



THE FACE 19 

the nerve sheath or into the stylomastoid canal. Facial paralysis 
may also arise from locomotor ataxia, the lesion being in the pons, 
and from hysteria. All these forms are very rare, comparatively 
speaking. The cerebral or medullary lesions which produce uni- 
lateral facial paralysis usually result from hemorrhage and tumor. 

The determination that facial paralysis is due to a peripheral 
neuritis or pressure may be impossible at the first visit of the patient, 
if this visit is made, as it usually is, within a few hours of the onset 
of the malady; but the peripheral form separates itself from facial 
paralysis of cerebral origin in the course of ten days or two weeks, 
for, if the nerve is inflamed or pressed upon in the foramen, the 
muscles of the face speedily undergo degeneration, because they are 
cut off from their trophic centres. 

In the cerebral form, on the other hand, the trophic changes do 
not occur, and the reactions of degeneration fail to appear, because 
trophic impulses can still reach the facial nerve trunk and the 
muscles which it supplies. In other words, electrical response in 
the paralyzed side remains normal in centric lesions and is lost 
in peripheral lesions. The only other conditions in which there 
can be developed the reaction of degeneration and the lesion not be 
in the nerve trunk or foramen is when there is a tumor at the 
base of the brain involving the facial fibers below the facial nucleus 
or destroying the nucleus itself. 

Very rarely in cerebral facial paralysis is the loss of power as 
complete as it is in the peripheral form. Again, in cerebral facial 
paralysis the eye on the paralyzed side can usually be closed and 
the forehead wrinkled, whereas in the peripheral form it cannot. 
Why this should be so is not clear, unless it is that in the muscles 
used commonly in pairs, as in those of the forehead, there is an 
adequate nerve supply through direct non-decussating tracts which 
innervate the muscles. When facial paralysis has associated with 
it none of the signs of peripheral wasting, and none of the remote 
causes of hemorrhage, embolism or thrombosis, such as result from 
impaired bloodvessels or a diseased heart, and when the paralysis 
comes on gradually (though it may be sudden from surrounding 
inflammation), the condition is probably due to cerebral tumor. 
This diagnosis is confirmed by the gradual spread of the paralysis 
to other parts, as the arm and then the leg on the same side of the 
body, and by the development, often before each additional spread of 
the paralysis, of a convulsion. 

The facial paralysis resulting from tumor at the base of the 
brain differs from that due to cerebral tumor or hemorrhage 
by the fact, already stated, that the reaction of degeneration 
quickly develops in the paralyzed part; that the parts supplied 
by the upper branch of the facial are often quite as much para- 



20 THE FACE AND HEAD 

lyzed as are those supplied by the lower branch, which is rare 
in the cerebral lesion; and there will commonly be found other 
evidences of a growth which, in a region so densely filled with 
important centres, speedily affects other functions. Thus in asso- 
ciation with this form of facial paralysis there will nearly always 
be found paralysis of the oculomotor nerve, causing ptosis, a mod- 
erately dilated pupil, and external squint, and there may also be 
paralysis of the abducens or sixth nerve, which causes ' internal 
squint by paralysis of the external rectus muscle. (See Ptosis.) 
The optic nerve may show choked disk, and there may be disturb- 
ance of vision. (See chapter on the Eye.) If the tumor is large, or 
is so placed as to involve the facial fibers for both sides as well as 
those of the oculomotor, abducens, and optic nerves on both sides, 
all these symptoms become, of course, bilateral. 

Facial palsy associated with deafness may indicate cerebellar 
tumor, the diagnosis of this cause being decided by the other cere- 
bellar symptoms, such as the peculiar gait. (See chapter on Feet 
and Legs.) Such growths are not uncommon in children. 

Sometimes very shortly after birth the child is seen to have a 
facial paralysis resulting from pressure by the forceps, which have 
slipped and injured the facial nerve, or have caused an extravasation 
of blood into the neighborhood of the parotid gland, thereby causing 
pressure on the nerve. The prognosis is usually favorable if due 
to such causes; but if the forceps have caused facial palsy by pro- 
ducing a cerebral hemorrhage, the outlook is bad. 

The possibility of facial paralysis being due to hysteria should 
not be forgotten. The loss of power under these conditions may 
be unilateral or bilateral, generally the former. Its association with 
the symptoms of hysteria described in the chapter on the skin, and 
elsewhere in this book, will aid in making the diagnosis. 

There yet remain to be considered several forms of facial par- 
alysis unilateral in character yet associated with paralysis elsewhere. 
These are, as follows : 

Unilateral facial paralysis very rarely occurs in association with 
monoplegia in acute anterior poliomyelitis. So seldom does it occur 
in this connection that it has been denied an existence. Often it is 
but temporary, while the monoplegia of the arm is permanent. It 
occurs more commonly with the disease in adults than in children. 

Facial paralysis with arm paralysis of the same side, followed in 
a short time by paralysis of the leg of the opposite side, is quite a 
characteristic symptom of syphilitic arteritis at the base of the 
brain. 

Crossed paralysis — that is, paralysis of the face on one side, and 
of the arm and leg on the other — is due to a lesion in the pons above 
the decussation of the pyramids and below that of the facial fibers 



THE FACE 



21 



(Fig. 5). Thus it is seen in this figure, on the left side, third in- 
scription, that the lesion in the pons cuts off the motor fibers in the 
place indicated, thereby causing the distribution of the paralysis 
just named. (See also chapters on Hemiplegia and on the Arms 
and Hands.) 

Sometimes the muscles supplied by the facial nerve escape par- 
alysis, but those of the jaw — namely, the masseters and temporals — 



Cortical centre for op- 
postte leg 



Lesion of cerebral mo- 
noplegia (brachial) 



Lesion of ordinary 
hemiplegia 



Lesion of cross paralysis 
(face of same side with 
limbs of other side) 



A lesion causing paraplegia 



A lesion causing hemi- 
paraplegia 




C'irliriil centre for op- 
posite arm 



Cortical centre for op- 
posite side of face 



Internal capsule (pos- 
terior limb) 



Motor nerve to face 

Decussation of pyra- 
mids 

Crossed pyram idal tract 



Motor nerves to upper 
limb 



Crossed pyramidal tract 



Sensory nerves entering 
cord, and decussating 
soon after entry 



Motor nerves to lower 
limb 



Fig. 5. — Diagram to show the general arrangement of the motor tract and the effect 
of lesions at various points. (Ormerod.) 



become paralyzed either bilaterally or more commonly unilaterally. 
This is a rare affection, and depends upon paralysis of the inferior 
maxillary branch of the trifacial nerve. This may be due to 
pressure produced by growths or inflammatory processes at the base 



22 THE FACE AND HEAD 

of the skull. It may also occur as the result of hemorrhage into 
the medulla, or from progressive bulbar paralysis. 

Ptosis. — In connection with the subject of facial paralysis that of 
ptosis, or drooping of the upper eyelid, must be considered (Fig. 7). 
It depends upon loss of function of the oculomotor nerve or its 
nucleus. Ptosis is a symptom of the greatest importance, first, 
because it is so readily recognized; second, because it is a source of 
great annoyance and alarm to the patient; and, third, and more 
important, it often aids us greatly in localizing lesions. 

The presence of this symptom should call to the physician's mind 
the various causes which produce it. In the first place it sometimes 
occurs as a congenital defect, and in such a case the history of the 
patient renders the diagnosis easy. 

If a congenital defect is not responsible for the ptosis it must 
depend upon disease affecting the oculomotor nerve itself or its 
nucleus. If the disease be sufficient to cause entire loss of 
function, we find, in addition to ptosis, that there is paralysis 
of all the external muscles of the eye except the superior oblique 
and external rectus, and in addition there will be a moderately 
dilated pupil, which will not contract, and paralysis of the 
ciliary muscle — that is, loss of accommodation. The eye can be 
moved outward by the action of the external rectus, and a little 
downward and inward by the superior oblique. Diplopia is 
present, and a little exophthalmos may be present owing to the action 
of the superior oblique, which presses on the ball. If the lesion be 
in the oculomotor nucleus, the near position of the nuclei of the fourth 
and sixth nerves will probably cause them to be affected also, thereby 
causing a general ophthalmoplegia (Fig. 6). If the lesion is not 
nuclear it is due to disease in the nerve itself, as already pointed 
out. If this is the case the lesion is probably due to pressure in the 
cavernus sinus or to periostitis of the bones forming the sphenoidal 
fissure through which the nerve passes. (See Plate I.) Sometimes, 
however, the paralysis of the nerve may be only partial, so that the 
external muscles of the eyeball escape, and only ptosis and a dilated 
pupil are present. Very rarely ptosis results from a cerebral hemor- 
rhage, without the other signs of oculomotor paralysis being present. 
That is to say, the branch of the oculomotor which supplies the 
levator palpebral is affected, while the branches supplying the 
external and internal ocular muscles escape. 

If there is a history of a cerebral attack resembling a mild apo- 
plexy, and a unilateral ptosis is present, the lesion is probably in 
the cortical centre for the oculomotor nerve in the angular gyrus 
just below the interparietal fissure. The lesion is, of course, upon 
the side of the cortex opposite the ptosis. Such a case is very 
rare. 



PLATE I. 




Base of Skull, showing the Oculomotor Nerves (III) Passing through the Sphenoidal 
Foramen. (Modified from Arnold.) 

The other cranial nerves are also numbered, and it is easy to see how an inflammatory exudate at 
the base might involve many of them. 
III. The oculomotor nerves. IV. The pathetic nerves. V. The trifacial nerves. 
VI. Abducens. VII. The facial nerves. 



THE FACE 



23 



A fourth cause of ptosis is due to an affection of the sympathetic 
nerve, and is sometimes called pseudoptosis. There are associated 
symptoms of vascular dilatation, with redness and swelling of the 
skin of the affected side, elevation of temperature in that part, con- 
traction of the pupil on the affected side, and apparent shrinkage of 
the eye into the orbit. This form of ptosis results from the paralysis 
of the unstriped muscular fibers of Muller which exist in the orbital 
fascia, for as these muscular fibers aid in holding open the lid their 




Fig. 6. — Showing the nearness of origin of the oculomotor (3), pathetic (4), and adducens 
(6). The roots of these nerves are shown by an incision which has divided the pons. III. 
The third nerve, arising from several roots. IV. The fourth nerve. VI. The sixth nerve, 
arising from three roots. (Modified from Arnold.) 

paralysis results in partial ptosis. Nothnagel asserts that such 
symptoms occur with lesions in the corpus striatum. 

A fifth cause of ptosis is reflex irritation usually through the 
fifth nerve. This is probably due to an inhibition of the oculomotor 
centre^ It is usually only transient. 



24 THE FACE AND HEAD 

Sixthly, it is not uncommon in cases of nervous syphilis for so- 
called alternate ptosis to develop (Fig. 7). First one eye is affected 
by ptosis and then the other just as the first begins to improve or 
recover. 

Ptosis has been known to complicate tetanus, probably as the 
result of reflex irritation of the fifth nerve. 

Ptosis, either unilateral or bilateral, may arise from hysteria and 
idiopathic muscular atrophy. If from hysteria the diagnosis can 
be made from the age, sex, and history of the patient, from the 
presence of hysterical sensory changes described in the chapter on 
the Skin, and from the fact that there is a tendency to spasm of the 
orbicularis muscle when the patient is made to look up. This con- 
traction of the orbicularis proves that there is no true paralysis of 
the levators. If the ptosis is bilateral and hysterical the head is 
tipped back when the patient is told to look up. 




Fig. 7. — Ptosis in a case of alternate hemiplegia of syphilitic origin. (Dercum.) 

Single or double ptosis is by no means a rare symptom of loco- 
motor ataxia, and is often associated with other evidences of oculo- 
motor palsy. Sometimes diplopia due to this disease is the first 
symptom complained of, and the patient may state thaf the diplopia 
comes and goes. 

Bilateral ptosis, like unilateral ptosis, may arise from tuberculous 
or syphilitic changes about the base of the brain owing to pressure 
on the cranial nerves (see Plate I), or it may be congenital, or if 
transient be caused by poisoning by gelsemium or conium. It is 
also seen in slight degree in feeble, overworked women, particularly 
in the early morning on awakening. 

Again, it is not very rare to see slight drooping of both lids in all 
the members of a family, in which case the condition is usually most 



THE FACE 25 

marked in the women, and is to some extent combated by the frontal 
muscles, which, in contracting, make the patient frown and draw up 
the eyebrows. (See chapter on the Eye.) 

Ptosis, with hemiplegia of the face and limbs, on the opposite side 
of the body, associated it may be with hemianesthesia, is due to a 
lesion in the crus cerebri, provided the two sets of paralysis occur 
simultaneously, otherwise they may be due to two separate lesions. 
(Hugh lings Jackson.) 

A very rare condition, of which there are but 27 cases on 
record according to Darquire, is recurrent 'paralysis of the oculo- 
motor nerve on one side. The attack begins with violent pain on 
one side of the head, nausea, and vomiting, and these symptoms 
are followed by ptosis, external strabismus, mydriasis, paralysis of 
accommodation, and crossed diplopia. It is seen most frequently 
in women, but may date from as early a period of life as eleven 
months. The attacks may last for a few weeks, and recur often or 
only after a lapse of many years. 

As already stated, a form of alternate ptosis sometimes also 
develops in syphilitic persons. 

Bilateral Facial Paralysis. — Bilateral facial paralysis is a rare con- 
dition, and when it occurs can only be due to a bilateral lesion in 
the cerebrum, to acute bulbar paralysis, to progressive bulbar par- 
alysis, to a lesion in the pons just where the facial fibers decussate, to 
bilateral disease of the pons owing to disease of the basilar artery, 
syphilis at the base of the brain producing a tumor or inflammatory 
thickening, very rarely to bilateral inflammation of the stylomastoid 
foramina, resulting from cold or double otitis, from toxic multiple 
neuritis, but not from that toxic neuritis due to alcohol. Very rarely 
bilateral facial paralysis results from multiple neuritis in its diph- 
theritic form. 

The development of bilateral facial paralysis due to a double 
cerebral cortical lesion never occurs without evidences of paralysis 
elsewhere in the body, such as monoplegia or hemiplegia. 

The bilateral paralysis of the facial nerve in acute bulbar par- 
alysis is characterized by the limitation of the paralysis, as a rule, to 
the neighborhood of the lips, by dysphagia, lingual paralysis, affected 
speech, paralysis of the ocular muscles, and a rapid pulse. This 
disease is very rare, and depends for its existence upon an acute 
inflammation or myelitis of the medulla oblongata. 

When due to progressive bulbar paralysis (glossolabiopharyngeal 
paralysis) the paralysis is confined chiefly to the lips, and is asso- 
ciated with alterations in the tongue (see chapter on the Tongue) and 
speech, with tremor of the tongue and stiffness of the lips. The 
mouth stands half-open, the lower lip is pendulous, and the patient's 



26 THE FACE AND HEAD 

expression is that of a person about to burst into tears. The symp- 
toms of glossolabiopharyngeal paralysis may, however, be exactly 
reproduced by diphtheritic paralysis, with this diiference in prog- 
nosis : the first type always die and the second type usually get well. 

In making a diagnosis of bulbar paralysis it should be remembered 
that another condition exists in rare instances in which no definite 
pathological changes can be found in the nuclei in the medulla 
oblongata, and yet many of the symptoms manifested by the patient 
are identical with those of glossolabiopharyngeal paralysis (true 
bulbar paralysis). This condition has been called " asthenic bulbar 
paralysis," and in it we find, as early symptoms, that the muscles of 
swallowing and of speech become easily tired on exertion, showing 
failure of the nuclei of the fifth nerve; that defects in articulation and 
speech are developed, indicating disorder of the nuclei of the ninth 
and tenth nerves; and clumsy movements of the tongue are present, 
which is a sign that the nuclei of the hypoglossal and twelfth pair 
are involved. These symptoms are practically identical with those 
of true bulbar paralysis. What are the symptoms which by their 
presence in the true disease and their absence in asthenic bulbar 
paralysis aid us in separating the two affections? The answer to 
this question is that the drooling of saliva, the atrophy of the tongue, 
lips, and extremities, the fibrillary twitching of the affected muscles, 
and the loss of electrical irritability in these muscles, all of which 
symptoms belong to true degenerative bulbar paralysis, are not to 
be found in the so-called asthenic form. There is, however, in the 
latter disease a condition rarely found in the degenerative form, 
namely, paralysis of the oculomotor, the lower facial, and the inferior 
division of the fifth or trifacial nerve, causing dilated pupils, diplopia 
(which, however, is not accompanied by strabismus), and ptosis 
(from the oculomotor failure), facial paralysis about the mouth (from 
facial nerve failure), and loss of expression about the eyebrows and 
forehead (due to facial and trifacial failure) . Whether the diagnosis 
be true degenerative bulbar paralysis or the asthenic form just 
discussed, in both the prognosis is most unfavorable. Indeed, the 
asthenic form is often the more rapidly fatal of the two. In the 
latter the nuclei in the pons are probably always involved, but, as 
already stated, no pathological changes have been demonstrated in 
any of these nervous centres. 

A very rare affection is oculofacial paralysis, which is congenital 
or develops in childhood, and is chronic. There are present par- 
alysis of the facial muscles and ptosis. 

Facial Spasm. — Spasm of the facial muscles may result from 
functional and organic disease, and occurs far more frequently in 
women than in men. The cause of the functional forms we do not 



THE FACE 27 

understand, as they occur in neuropathic persons and about the 
climacteric period. Rarely the spasm arises from reflex irritation 
through the trifacial nerve, resulting from a decayed tooth or a cause 
in the eye or in the skin. Habit spasm arises from an acquired 
trick. The organic causes are many. Thus there may be an irri- 
tative lesion of the facial nerve trunk or one in the cortical centre for 
the face, a tumor pressing on the nerve at its point of origin, or an 
aneurysm of the vertebral artery. The spasm may be confined to 
one side or distributed over both sides, and may be clonic or tonic in 
type. Sometimes it occurs only on attempted movement; in other 
eases it is constant. The clonic form is the more common. 

Spasm of the face is seen in chorea, convulsive tic, blepharofacial 
spasm, in tetanus, meningitis, and epilepsy. When due to chorea 
it nearly always is clonic or twitching, as it is also in convulsive 
tic and habit spasm, but in tetanus, meningitis, and epilepsy it is 
generally rigid or tonic. In chorea the spasm is most marked about 
the corner of the mouth and the eyebrow or eyelids. The move- 
ments of convulsive tic are exceedingly sudden, darting across the 
face and involving all the muscles supplied by the facial nerve. As 
a rule this affection is unilateral. These spasmodic movements of 
convulsive tic may be almost constant or appear in paroxysms, and 
rarely the muscles of the jaw, the neck, and tongue are affected. The 
disease depends upon a disorder of the facial nerve, or its centre-, 
which is not understood. The prognosis is bad so far as cure 
is concerned. Spasm of the levator palpebral superior^ muscle i> 
sometimes seen as a symptom of exophthalmic goitre. It is called 
" Abadie's sign." 

In blepharofacial spasm there are paroxysmal spastic contrac- 
tions of the orbicularis palpebrarum and other facial muscles. The 
spasm often tightly closes the lids. Generally in children there i- 
also photophobia with the spasm of the eyelids, which is often tonic 
in character and generally bilateral. This condition has associated 
with it what have been called "Graefe's spots," 1 namely, the pres- 
ence of spots near the supra -orbital foramen or over the vertebra 1 , 
which when pressed on cause sudden relaxation of the spasm. These 
should always be sought for, as they aid in giving relief to the 
patient. 

Spasmodic movements about the eyes such as have just been 
described are sometimes paralleled by what is called nictitating or 
clonic spasm, which is probably due to some undiscovered cause of 
reflex irritation. 

1 This term should not be confused with the more common term "Graefe's sign," used to 
indicate the condition in exophthalmic goitre, in which the lids fail to follow the eyeballs 
when the patient looks down. 



28 THE FACE AND HEAD 

The development of facial spasmodic twitching accompanied by 
a sudden burst of explosive speech, repeating the last word heard 
or said by the patient in conversation (called echolalia), or the 
sudden bursting out with some blasphemous or filthy word (called 
coprolalia), is sometimes seen in neurotic adults or children, and 
is often associated with perversion of moral sense. It is called by 
Gilles de la Tourette "Maladies des tic convulsifs," but this is an 
unfortunate term, because it is apt to be confused with ordinary 
convulsive tic of children or adults. (See Electric Chorea and 
Myoclonus Multiplex in the chapter on the Hands and Arms.) 

In tetanus the muscles of the jaw, the masseters and temporals, 
are first involved in the tonic contractions, and these are followed 
by rigidity of the muscles of the neck and body. Often the risus 
sardonicus is marked from the first, and the face soon looks like 
that of an old man owing to the muscular contractions. 

In meningitis the characteristic symptoms which label the malady 
render facial spasm a comparatively unimportant symptom, and in 
epilepsy the convulsive seizure soon makes easy the diagnosis of 
the cause of the facial spasm unless the epilepsy is limited in its 
character, when the history of the presence of an aura, or of uncon- 
sciousness, or biting of the tongue may be discovered. 

Spasm or contractures of the muscles of the face sometimes fol- 
low facial paralysis as recovery begins, and the contractures involve 
the formerly paralyzed muscles, whereas in paralysis in the limbs 
the contractures generally take place in the muscles which are not 
paralyzed. Sometimes these contractures in the face are permanent, 
and are due to incomplete restoration of the functions of the muscles 
affected. 

Care should be taken to remember that not very uncommonly 
contractures in the muscles of the face result from hysteria, and 
that they are often on the side opposite the facial paralysis if the 
latter exists. 

Active spasm of the muscles of the face may follow exposure to 
cold, and it sometimes follows the paralysis due to this cause, or, in 
other words, is a sequence of Bell's palsy. 



THE HEAD AND NECK. 

In examining the head we look for variations from the normal in 
its shape, its fontanelles if the patient is a young child, the position 
in which it is held, and its movements as governed by the cervical 
muscles. Of the last I shall speak first, although they have been 
mentioned under the heading of wryneck. The head is moved 



THE HEAD AND NECK 29 

abnormally in nodding spasm, in chorea, and in tetanus and strych- 
nine poisoning. It is also thrown backward and forward or 

from side to side in epilepsy, and in hysteria or in the convulsive 
seizures occurring in young children. 

Nodding Spasm. Nodding spasm of the head, depending upon 
somewhat rhythmical contractions of the sternomastoid and trape- 
zius muscles, is sometimes seen in half-fed or rickety children. It 
also occurs in hysterical women, and in men who are not hysterical. 
The nodding may be slow and infrequent, only coming on with 
excitement, or it may be practically constant. It always becomes 
worse when the patient is examined, and may be so rapid and forcible 
as to seem almost severe enough to shake the head off the shoulders. 
Often the muscles involved will be found very rigid. 

If the spasmodic movement be not rhythmical, as it usually i> in 
nodding spasm, and yet be more or less constant though irregular, 
the cause is probably chorea minor if it is present in a child, or it 
may belong to the irregular movements of adults classed under the 
various forms of tic or choreiform spasm. (See chapters on the 
Hands and Arms and on Convulsions and Spasms.) 

Wryneck consists in a drawing of the head to one side by spasm 
of the sternomastoid muscle, and at the same time the head may 
be tilted backward or forward according to the accessory muscles 
which may be involved in the spasm. 

Sometimes a tonic spasm of the sternomastoid muscle, produced 
by exposure to cold or due to a distinct nervous lesion, causes the 
head to be drawn down over the shoulder, or bilateral spasm of this 
muscle causes fixation of the head. If the cause be exposure, witli 
resulting myositis, the history of exposure, combined with that of 
a sudden onset, will permit a correct diagnosis and a favorable prog- 
nosis, it being remembered, however, if the patient is a female, that 
hysterical spasm may be the cause. If hysteria is the cause, the 
history of the patient, the presence of alteration in her color fields 
and the other signs of hysteria can probably be elicited. (See chapters 
on the Eye and on the Skin.) On the other hand, if the contraction 
has come on gradually, after some injury or in association with 
some nervous affection elsewhere, it is probable that a true nervous 
lesion underlies the disorder. 

If it is a tonic spasm the involved muscle is on the side toward 
which the head is drawn, and the muscle on the opposite side is seen 
to be prominent owing to its being stretched by its opponent. The 
chin is, moreover, directed upward and away from the affected side. 
Rarely the trapezius is the only muscle involved, in which case the 
head is drawn backward and toward the diseased side, or, if the 
sternomastoid and trapezius muscles are both involved the head is 



30 THE FACE AND HEAD 

tilted laterally and backward until the patient • looks up in the air. 
Pain in the muscles only occurs from fatigue. This tonic spasm 
affecting the muscles which support the head can be separated 
from that occurring in tetanus by the fact that in tetanus there is a 
general diffusion of the spasm to other muscles, although in that 
form of tetanus called "head or cephalic tetanus" the diagnosis 
is more difficult. 

Cephalic tetanus usually has the following diagnostic points : there 
is a history of infection, the character of the onset is sudden, there 
are trismus, difficult swallowing, respiratory disturbance, and facial 
paralysis with rare involvement of the ocular muscles. The spasm 
in cephalic tetanus is also often increased by movement or by the 
attempt to take food. Strychnine poisoning is also to be thought 
of, but the limited character of the convulsion excludes that con- 
dition. Should the muscles be affected by a clonic spasm the 
head is jerked about instead of remaining fixed. 

Retraction of the head in children is an indication in many cases 
of serious brain disease, and commonly arises from a basal menin- 
gitis. It is to be remembered that some of these cases recover, 
though such a result is rare. Again, we should not forget that caries 
of the cervical vertebra? may cause this position, or that tender and 
enlarged glands in the neck may produce such a result. Sometimes, 
too, it occurs after falls without there being any other indication of 
meningeal irritation. Rarely in neurotic babies retraction of the 
head, as a temporary symptom, accompanies attacks of indigestion. 
Similarly in adults suffering from cerebrospinal fever the head is 
often held in a retracted posture. 

The posture of the head may also aid us in diagnosis when no 
spasm of its governing muscles exists. Thus, chronic deafness in 
one ear may cause the patient to hold one side of his head further 
forward than the other, in order to catch the sounds he seeks with 
the good ear, and pronounced strabismus may cause a child to so 
carry its head as to improve its sight and avoid diplopia. 

Persons suffering from great mental depression with a tendency 
to melancholia often sit for hours with the head bowed forward with 
the chin resting on the chest. 

The changes from the normal in the shape of the head are to a 
certain extent considered in that part of this chapter dealing with 
the symmetry and appearance of the face, but there still remain to 
be discussed the changes in the shape of the head as a whole. These 
occur in acromegaly, osteitis deformans, and in hydrocephalus, 
microcephalus, rickets, idiocy, myxedema, and cretinism. 

The head of hydrocephalus is greatly enlarged above the level of 
the ears, and this causes the face, already having a tendency to faulty 



THE HEM) AS I) NECK 3] 

development, to look small and wizened. The eyes seem somewhat 
bulging, the orbital plates are oblique, and the back of the head 
is flattened. Sometimes in true hydrocephalus the fontanelle re- 
mains pulsating for a long period. Again, in true hydrocephalus 
choked disk is sometimes manifested quite early. (See Chvostek's 
and Trousseau's Signs.) In microcephalia, on the other hand, the 
head is small and often narrow. Technically, the term micro- 
cephalus is applied to idiots whose heads are less than seventeen 
inches in circumference. Nearly always the head of an idiot is ab- 
normally formed. 

The cretinoid head is large, heavy, and massive. 

When a young child has unusually prominent parietal and frontal 
bones, which seem bulging, and there is a general resemblance 
in the shape of the skull to that of hydrocephalus, we suspect the 
presence of rickets. As a rule, the forehead is broad and high, the 
top of the head flat, and the shape of the head more round than in 
the genuine disease. Sometimes in such a child we find, in addition 
to these changes from the normal, spots of thinned bone in the 
occipital and parietal regions. These may be also somewhat soft- 
ened, and this condition, called "craniotabes," is usually a sign of 
rickets which exists in association with infantile syphilis. Rickets 
is seen nearly twice as often in boys as in girls, and there is usually 
to be found deficient development of the bones everywhere, particu- 
larly in the ribs and legs. (For the rachitic rosary, see chapter on 
the Thorax.) 

The condition of the fontanelles in young children is of impor- 
tance in diagnosis. In the healthy child all the fontanelles save 
the anterior fontanelle close during the early weeks after birth, but 
the latter opening does not close entirely until the infant is about one 
year and a half old. During the first few months this fontanelle 
closes very slowly indeed, but after this time has elapsed its edges 
become rapidly approximated. The presence of other fontanelles 
in a child's skull after it is several months old indicates rickets, 
syphilis, hydrocephalus, or some intracranial growth producing 
pressure on the cranial bones, preventing their approximation. 
Generally, however, these minor fontanelles are not found open but 
closed, and the condition of the anterior fontanelle is the guide in 
diagnosis. In severe cases of rickets the anterior fontanelle remains 
open until the third or fourth year, and should the rachitic tendency 
be developed early in life the edges of the fontanelle may not only 
fail to be approximated, but may actually recede from each other. 
Sometimes if the edges of the fontanelle are found to be softer than 
usual the diagnosis of rickets can be so confirmed. If syphilis be 
the cause of the deficient bone development, evidences of this disease 



32 



THE FACE AND HEAD 



in mucous patches about the mouth and anus may be found or a his- 
tory of heredity adduced; while if the condition be hydrocephalus 
the fontanelle will be markedly bulging. 

If the skin over the fontanelle be found to be bulging temporarily 
to a slight extent, the cause probably lies in some acute disease with 
fever, producing cerebral congestion; whereas, if permanent, and 
if the general dimensions of the skull are not increased, an intracra- 
nial growth may be the cause, or a cerebral hemorrhage, a purulent 
meningitis, or some cystic formation may be present, or sometimes 
a thrombosis of a cerebral sinus produces hydrocephalus and bulg- 
ing. In other cases thrombosis causes sinking-in of the fontanelle. 
This difference in the tension of skin over the fontanelle aids us, in 
separating the meningeal symptoms of pneumonia from those of 
true meningitis, for in the true form the scalp is tense and in pneu- 
monia it is often retracted. 

Marked sinking in or collapse of the fontanelle always indicates a 
grave condition arising from some disease which seriously weakens 
the heart and general circulatory system, particularly marasmus and 
cholera infantum. The other symptoms associated with this state 
are usually a sunken appearance of the eyes, slight duskiness of the 
face, a cool skin, and a rapid, feeble pulse. The patient is almost 
comatose, and there may be slight convulsive seizures. Such a 
condition has been called the " hydrocephaloid state," and has been 
confused with symptoms of cerebral effusion arising from tuberculous 
meningitis. 

If there be marked diarrhea present the following table of Symes 
will serve to clear the diagnosis : 



Hydrocephaloid State from Diarrhea. 

Diarrhea. 

No ocular paralysis. 

No rise of temperature. 

No headache. 

No tension or bulging of fontanelle. 

No rigidity and 

No retraction of head. 



Cerebral Effusion (as in Tuberculous 
Meningitis). 
Constipation. 

Ocular paralysis and squint. 
Slight feverishness. 

Headache (if old enough to complain). 
Bulging fontanelle. 
Rigidity and retraction of head in many cases. 



Sometimes in rachitic babies auscultation of the fontanelle will 
reveal a murmur, hemic in origin. This murmur can, however, 
occasionally be heard when no such disturbance of nutrition exists. 

Excessive sweating of the head, producing a wet pillow, is often 
an indication of rickets when it occurs in a child. 

A swelling in the neck in the median line, or on both sides of the 
median line, anteriorly, is probably due to goitre. If it is associated 
with cardiac palpitation and distress, exophthalmos t tremor , ner- 



mi-: jii;m) and neck 



33 



vou.sne.ss, and depression of spirits, it is called exophthalmic goitre 
(Fig. 8). If these symptoms are absent, the condition is simply 
one of overgrowth of the thyroid gland. 

Aside from swelling of the glands of the neck due to syphilis, 
Hodgkin's disease (see chapter on Fever), struma, and tuberculosis, 
there may be enlargement of the parotid gland on one or both sides, 
just in front of the ears and extending under the angle of the jaw. 
This swelling may be due to the specific inflammation involving 




Fi<;. 8. — Exophthalmic goitre. (Meltzer.) 

these glands, known as mumps, or be due to other infections, such 
as typhoid, typhus, and pyemic fever. If the latter be the cause, 
suppuration usually ensues. Rarely enlargement of the parotid 
glands follows trauma or disease of the abdominal viscera or pelvic 
organs. Sometimes the enlargement is chronic after the acute in- 
flammation is passed by. 

(For the movements of the head in epilepsy and hysteria, see 
chapter on Convulsions.) 



CHAPTER II. 

THE HANDS AND ARMS. 

The general appearance of the hands and arms — The shape of the hands in 
disease — Spasms of the fingers— Tremors of the hands — Paralysis of the 
hands and arms. 

Inspection of the Hands. — The appearance of the hand and arm 
often gives us valuable hints in the diagnosis of disease, chiefly by 
reason of variation in their shape, manner of movement, and general 
consistency; but as all these conditions vary widely in normal individ- 
uals, we can only regard distinct and well-marked alterations from 
the normal type as indicative of a definite disease. We can, however, 
often gather general information as to the patient from the hands, 
particularly as to his occupation; thus we see the smooth, soft hand of 
the professional man or clerk, the horny hand of the laborer, the 
blackened nails and skin of the machinist, or the blue-black dot- 
tings of the hand of the miner; and Hirt asserts that atrophy of the 
antithenar eminence often ensues in cabinetmakers, perhaps from 
the excessive use of the plane. Even when no pathological condition 
exists we are wont to regard the heavy and somewhat thick and clumsy 
hand as an evidence of a phlegmatic temperament, and the thin, 
wiry, dexterous hand as indicative of the nervous temperament. 
Similarly, we recognize as the hand of the strumous that one in which 
the fingers are slender between the joints and the joints themselves 
thick and clumsy, or, again, in persons with tuberculous tendencies, 
we see a slender, delicate hand, easily compressed and somewhat 
effeminate in type. Very commonly, too, in children who have 
developed heart disease in early life the hand becomes square 
looking, and the fingers are club-shaped through thickening at the 
tips. A similar clubbing also manifests itself in many cases of 
emphysema and chronic phthisis in adults, and unilateral clubbing 
with incurvation of the nails of one hand is sometimes seen in 
thoracic aneurysm. 

From the appearance of the nails we can often gain important 
information; thus, whenever the color of the blood in the capillaries 
under the nails is dusky we know that a deficient pulmonary func- 
tion exists or that the circulation is impaired, it may be from feeble- 
ness or from cold. In anemia the nails are often very pale, and 
Stephen Mackenzie has asserted that if pressure on the tip of the 



INSPECTION OF THE HANDS 35 

finder completely empties the capillaries under the nails so that the 
appearance is pale the red corpuscles are present in only half the 
usual number. 

White spots in the nail may he due to injury of the matrix by 
picking at the base of the nail, or be due to acute fevers producing 
trophic changes. 

When the nails are striated and in longitudinal ridges the patient 
is often of the gouty diathesis, while transverse ridges may indicate 
arrest of nail growth through local injury to the matrix or the 
impairment of the general nutrition as the result of some severe 
systemic shock, such as a severe surgical operation or prolonged 
illness. Sometimes these marks result from a severe attack of 
gout, and Fothergill tells us that it took about seven months for 
such a mark to grow out of his nails. Ordinarily, this mark will 
be found about half-way up the nail three months after the attack. 
In hemiplegia or acute infantile palsy the growth of the nail of the 
paralyzed part is generally arrested, as can be determined by stain- 
ing it and watching it from day to day to see if the stained part 
gradually moves away from the base. When the nails are distorted 
and thickened the cause may be local injury or peripheral neuritis, 
or any condition of the nervous system resulting in decided trophic 
influences, as in that rare condition syringomyelia. 

Hypertrophy of the nails so that they are abnormally elongated 
is usually associated with thickening and the development of great 
fragility. The nail may even be spirally twisted (onychogyropho- 
sis), or, if very wide, may cut into the skin and produce paronychia. 
These conditions may result from skin lesions, such as eczema or 
lichen ruber, at or near the matrix, or be due to syphilis, and Yogi 
asserts that mere thickening may arise from severe fevers. They 
may also be seen in cases of Raynaud's disease, or in sclerodactyle, 
and in cases of pulmonary osteo-arthropathy. 

Atrophy of the nails may apparently arise from causes identical 
with those which produce hypertrophy, and Kaposi has seen the 
nails soft and membrane-like, with abscesses under them, from 
psoriasis of the fingers. 

A diagnostic indication given by the fingers is seen in dactylitis 
due to syphilis. Similar deformity, often multiple, also occurs in 
scrofulosis or tuberculosis. In other cases this is replaced by an 
eruption on the skin of the hand characteristic of syphilis. Another 
indication is seen in the ulcers at the bases of the finger nails, with 
ecchymotic spots on the skin, produced by the chloral habit; and 
still another is the sores seen at the bases of the finger nails in persons 
who handle irritating drugs, such as elaterium. (See chapter on 
the Skin.) 

Congested veins on the hand may indicate obstruction to the 



36 THE HANDS AND ARMS 

venous circulation of the arm, or general lack of vascular tone and 
a feeble heart. 

When the hand is cold and clammy the condition may be due to 
bromidrosis, or a local disturbance in innervation of the sweat 
glands. It is often seen in cases of so-called spinal irritation and 
nervous exhaustion. Excessive sweating of the hand is also often 
seen in cases of progressive muscular atrophy. 

There are two sets of movements associated with the muscles of 
the wrist and hand which possess grave prognostic and diagnostic 
importance in the presence of exhausting fevers. The first of these 
is twitching of the muscles of the forearm (subsultus tendinum). It 
indicates severe and dangerous disease. The second is picking at 
the bedclothes. The grave import of this dangerous symptom, 
"picking up the bedclothes," or carphologia, was recognized by 
Shakespeare in his description of the death of Falstaff: " After I 
saw him fumble with the sheets, and play with flowers, and smile 
upon his fingers' ends, I knew that there was but one way; for his 
nose was as sharp as a pen." Hippocrates has well emphasized the 
gravity of this symptom, for he says: "In acute fevers, in peri- 
pneumonias, in pleuritis, and in headaches the hands are moved to 
and fro about the face, seeking in the void, as if gathering bits of 
straw, picking at the coverings, or detaching objects from the walls 
of the room, constituting so many signs of a fatal termination." 

The fingers are often distorted and twisted out of their normal 
position from the trophic changes which take place in gout and 
arthritis deformans (rheumatoid arthritis). In gout the deformity 
invades the small joints in particular, and in many instances appears 
most marked in the forefinger. Fixation and deformity of the 
fingers occur through the deposit of urate of sodium in large amounts 
about the joints in their tendons and sheaths, so that the fingers 
are as in splints. The knobs of urate of sodium appear as hard, 
white masses, and, if very superficial, as glistening masses, the sur- 
faces of which often break down and allow the escape of material 
looking like powdered wet chalk. The joint surfaces themselves 
are not primarily much altered, but secondarily grave changes occur 
in them. 

Very commonly in gout the only joints of the hand which are 
involved are the first joints of the fingers, a knob developing on 
either side of the knuckle (Fig. 10). The little finger in gout is 
often bent at an acute angle at the middle knuckle, so that it is held 
in an awkward hooked position. This is most commonly seen in 
women, while in men it is common to see forced flexion of the first 
phalanx of the middle finger into the palm of the hand, even when 
very little if any deposit of urates has taken place. This drawing 
down of the fingers is considered by Paget to be pathognomonic 



INSPECTION OF THE If. Whs M7 

of gout, although the patient will claim that it is due to the use of a 
cane, a hammer, or other extraneous cause. 

Distortion of the hand with drawing of the finger or fingers into 
the palm may be due to Dupuytren's contraction, which results from 
burns or other injury to the palmar fascia. 

While the history of the patient, the localization of the manifes- 
tations of the disease, and its character render a differential diag- 
nosis between the hand of gout and that of arthritis deformans ;i 
possibility, it should not be forgotten that the deformities of gout 
may take every position assumed by those of arthritis deformans. 

In arthritis deformans the distortion of the hand may be far more 
marked than in gout, for here there is not a splint-like deposit about 
the joint, but in its stead the development of exostoses on the edges 
of the articular surfaces, which at once lock and disjoint the fingers, 




Fig. 9.— Arthritis deformans in a woman of twenty-one years. Characteristic distortion of 

ring finger on left hand and seal-fin hand on right side. (From the authors wards 

while at the same time the opposite side of the joint may be par- 
tially absorbed, so that dislocation is still more readily produced. 
As a result there is sometimes developed what is called the "seal-fin 
hand" (also seen in cases of gout), a hand in which the digits are 
deflected chiefly toward the ulna, through the action of the extensor 
muscles, which are supplied with nerves which are reflexly irritated 
by the condition of the joints, and thereby cause spasm (Charcot) 
(Fig. 9). 

The term Heberden's nodes is applied by some to the exostoses at 
the sides of the phalangeal joints met with in rheumatoid arthritis 
or arthritis deformans; by others, as by Duckworth, to somewhat 
similar gouty deposits. These are sometimes called "Haygarth's 
nodosities." 



38 



THE HANDS AND ARMS 



Chronic rheumatism may produce gradual changes in the shape 
of the hand chiefly through disuse and the alterations which it 
causes in the capsules and ligaments. The chief alteration is immo- 
bility or stiffness. Some persons believe that when the hand wastes 
it does so not from disuse, but through reflex nervous influences. 
Chronic rheumatism rarely, if ever, occurs in the hands alone, but 
when it does the joints are often swollen and somewhat tender, but 
never as hard as in gout. 

The finger- joints are not commonly involved in acute articular 
rheumatism, certainly very rarely as the only manifestation of the 
disease. The inflammatory process is more apt to be about the 





Heberden's gouty nodes, 
mon forms of terminal phalangeal deflection. 
Forefinger and little finger of a woman aged 
seventy years. "Crab's-eye" cysts over the 
joints are also depicted . (Duckworth .) 



Fig. 10. 
Illustrating com- Nodular swellings (Herberden's nodes) due 
to gouty arthritis on the forefinger and little 
finger of a woman aged fifty years. (Duck- 
worth.) 



ball of the thumb, or in the wrist and carpal joint. The hand is seen 
under these circumstances as a clumsy, swollen mass, puffy, and 
exquisitely tender and hot. Sometimes it is quite red at the joints, 
but otherwise quite pallid, particularly in the puffy, edematous area 
on the back of the hand. The presence of intense local inflamma- 
tion, the history of sudden onset, and the intense pain on movement 
readily separate acute rheumatism from chronic gout and arthritis 
deformans, and leave it to be separated from sprain, septic arthritis, 
and deep-seated inflammation of the hand proper. The first is 
excluded by the history, the second by the history and general lack 



IXSPECTIOX OF THE HANDS 30 

of evidence of gonorrhea or sepsis or purpura, and the third by the 
lack of accompanying general systemic disturbance and the absence 
of a history of traumatism or infection. In this connection it should 
not be forgotten that synovitis of the joints of the hands, wrists, and 
elbows sometimes occurs during the fall of temperature in scarlet 
fever, and is often not associated with any rise of temperature as a 
result of its development. The condition is sudden in onset and 
usually rapid in its course. The same state may exist in the joints 
of the lower limbs, but Marsden found it in the hands and wrists 
in 72 instances out of 100 cases, and only 25 times in the larger joints 
out of 100 cases. The condition usually appears, however, in rheu- 
matic children and those with a rheumatic heredity, and is generally 
relieved by salicylates, so it is not a pure septic arthritis. 

The nervous disturbances which change the appearance of the 
hands are very numerous. 

Angioneurotic edema is not peculiar to the hand, although fre- 
quently involving this part of the body. It consists of a swelling 
varying in size from a dime to a silver dollar, which is not edema- 
tous in the sense that it can be pitted on pressure. This swelling, 
which may be multiple, red in color, or pale and waxy in appearance, 
lasts but a few hours or days, disappears, and often speedily returns. 

Somewhat allied to angioneurotic edema is that condition of the 
hand (or toes) characterized by a white and waxy or slate color of 
the fingers, associated with coldness, swelling, and mottling of the 
skin, termed Raynaud? s disease. Often this is a passing condition, 
but in its severe forms there is finally developed dry gangrene 
in the fingers involved. The conditions of the hand resembling it, 
from which it must be separated, are senile gangrene, in which the 
advanced age of the patient and the presence of diseased and thick- 
ened bloodvessels will enable us to decide on the latter as the cause; 
frost bite, in which the history of exposure will be of value, although 
exposure to cold often precipitates an attack of Raynaud's disease; 
ergotism, which can be discovered by the history of the patient having 
for a long time taken food which may have contained bad rye; 
leprosy, which will probably be seen more marked in other parts, 
and in the patches of which can be found the leprous bacillus; and 
alcoholic neuritis, of which we shall speak later. (See chapter on 
the Skin). 

In that state known as Morvan's disease, or "pain anesthesia 
with whitlow," there is a slowly progressive loss of power in 
the hand, with atrophy and ulcers about the bases of the nails. 
Sometimes the terminal phalanges undergo necrosis, and enlarge- 
ment of the fingers, through swelling, may be very marked. It is 
probable that this condition represents two separate lesions, namely, 
neuritis and syringomyelia, and it is an exceedingly rare disease. 



40 THE HANDS AND ARMS 

Swelling of the hand, followed in some months by rupture of the 
skin, may, in a person from the tropics, mean mycetoma, which is, 
however, seen more commonly in the lower extremity as " Madura 
foot." 

In addition to these trophic changes in the hand we have the 
so-called "spade-like" hand seen in myxedema, acromegaly, and the 
pulmonary osteo-arthropathy of Marie. In myxedema the deform- 
ity depends upon the alterations in the subcutaneous tissues, rather 
than on changes in the bones, so that the hand is swollen or boggy 
looking, but does not pit on pressure as in true edema. In acro- 
megaly the enlargement is chiefly osseous, as it is also in pulmonary 
osteo-arthropathy, the formation being on a gigantic scale. In the 
latter disease, however, the hands and feet are alone affected, and 
the enlargement is not symmetrical. Further, this condition is 
nearly always associated with changes in the lungs, such as emphy- 
sema, tumors, and old bronchial troubles. The hands are not only 
greatly enlarged, but deformed, so that a side view of the finger tips 
reminds one of the shape of a parrot's beak, the nail being turned 
over the end of the finger. This is particularly well marked in the 
thumb. 

The differentiation of pulmonary osteo-arthropathy from acro- 
megaly is to be found in the fact that in the first-named disease there 
are no changes in the face, the skin, lips, or orbital ridges. Neither 
is there spinal kyphosis in the cervical region, although it may be 
present lower down. Again, in pulmonary osteo-arthropathy the 
long bones of the upper extremities are greatly enlarged in their 
epiphyses, while in acromegaly they are not so locally enlarged. 

Alterations in the contour of the hand are, however, far more 
frequently produced by atrophic processes than by those which 
result in hypertrophy. They arise in cases of paralysis not only 
from wasting of the muscular tissues, so that hollows or sunken 
places occur, but also from the distortions caused by the contrac- 
tions of healthy muscles, which, having no opposition as in health, 
speedily draw the bones of the hand into abnormal positions. In 
other cases the diseased muscular fibers may be spasmodically con- 
tracted, overcoming the resistance of the healthy muscles. 

The wasting of the hand seen in old age, particularly in women, 
and in advanced phthisis, diabetes mellitus, and other conditions in 
which the tissues of the body in general lose their plumpness, is so 
universally distributed that a diagnosis of wasting from old age is 
not difficult. On the other hand, the wasting due to nervous lesions 
is generally not universal, but limited to single muscles or groups 
of muscles, the remaining portion of the hand having its normal 
appearance or being only indirectly influenced. 

Under the name of "clawhand," or " main-en-griff e," we find 



INSPECTION OF THE HANDS 41 

a deformity of the hand which is in itself very characteristic, although 
indicative of several causes which all operate in an identical manner. 
The back of the hand loses its normal convexity and becomes some- 
what concave, the tendons on the extensor surface stand out in 
ridges, the proximal phalanges are drawn backward toward the 
wrist, while the second and third phalanges are drawn toward the 
palm of the hand (Fig. 11). Sometimes, however, the tips of the 
fingers are drawn toward the back of the hand. This deformity 
results from atrophy and paralysis of the interossei muscles and 
lumbricales, which are supplied by the median and ulnar nerves. 
The extensor communis digitorum and flexor digitorum produce a 
dorsal flexion of the first phalanges and a complete palmar flexion 
of the second and third phalanges. A certain amount of immo- 
bility is also caused by the fact that flexion of the hand is impossible 
in the fingers and almost lost at the wrist. 




Fig. 11.— Claw-hand. (Gray.) 

The clawhand having been recognized, it remains to be decided 
what are its causes. It may be due to disease of the peripheral 
nerves (the ulnar and median), of the cells in the spinal cord, and 
of the cells in the cerebral cortex in the hand area. 

Taking up for consideration paralysis of the median and ulnar 
nerves as a cause of clawhand, we find that the most common cause 
is a neuritis produced by some mechanical injury resulting from 
an accident, or from the following of some occupation in which, for 
example, the artisan presses his elbow constantly on some hard sur- 
face. The deformity may be, therefore, either unilateral or bilateral 
(generally the former), and there will be evidences of local injury, 
or a history which will indicate that the lesion is peripheral. Further 
than this, there will nearly always be found, in ulnar and median 
injury, sensory as well as motor paralysis; and Hirt asserts the 
remarkable fact that the clawhand may develop in cases in which 
sensory disturbances are the only evidence of median and ulnar 
difficulty — in other words, before motility is lost through paralysis. 



42 



THE HANDS AND ARMS 



(See chapter on the Skin, Anesthesia of the Skin.) Toxic neuritis 
very rarely, if ever, causes clawhand, as the musculospiral nerve is 
more commonly affected in this condition and the extensors become 
paralyzed. 

There are several spinal causes of clawhand, the most important 
of them being progressive muscular .atrophy, that disease in which 
there are atrophy and abnormal change in the anterior horns of the 
gray matter of the spinal cord, particularly in the cervical region 
(Fig. 12). It will be remembered, too, that the anterior nerve roots 
and motor nerves become involved in this process. As a result of 




Fig. 12. — Areas of spinal cord involved in progressive muscular atrophy. The areas involved 
are the anterior horns of gray matter chiefly (shading heavy) (1) and the anterior lateral 
tracts (2) and anterior root zones. The anterior nerve roots which arise from the anterior 
horns also atrophy, and the atrophy extends all the way to the nerve plates in the muscles — 
along the nerves. 

these changes, we have developed loss of power in the hand and 
arm followed by the development of a clawhand from wasting of 
the same muscles, as already described, the disease process being 
generally bilateral, but affecting the right hand and arm more than 
the left, as a rule. As progressive muscular atrophy often makes 
its first manifestation in these muscles, the hand affords much 
diagnostic information in suspected cases, and if the patient with 
this disease be watched as he unbuttons his coat, it will be found 
that he does not use his thumb and first finger, but pushes the buttons 



INSPECTION OF THE HANDS 



43 



or the edge of the buttonholes with the back of his fingers. The 
additional symptoms are pain or paresthesia in the affected parts 
prior to the wasting, and the spread of the paralysis, as its name 
indicates, from muscle to muscle (Fig. 13). Thus, beginning in 
the ball of the thumb it passes to the interossei and thence up the 
forearm and arm. Sometimes, however, the forearm muscles escape, 
and the shoulder muscles are attacked secondarily. Very rarely are 
the shoulder muscles first affected. Soon after this the dorsal mus- 
cles fail and lordosis begins, or the head falls forward on the chest. 
Finally, the respiratory muscles are attacked. The irritability of 
the muscles is increased, so that they contract if tapped, and 
fibrillary tremors constantly affect them in many instances. No 
vasomotor changes take place in the affected part, but, finally, 
the reactions of degeneration develop. The disease may last for 
many years. 

Sometimes in chronic poliomyelitis in the adult a deformity some- 
what like that of clawhand mav exist, but this is a vers' rare con- 




Fig. 13. 



-Hand aud forearm in chronic spinal muscular atrophy, showing especially wasting 
of thenar and hypothenar eminences. (Dercum.) 



dition, comparatively speaking, and is separated with difficulty 
from the clawhand of peripheral neuritis of a general and severe 
type. As the result of the acute poliomyelitis of infancy, we may 
also have the hand distorted by contractures, such as forced exten- 
sion in paralysis of the flexors, forced flexion in the paralysis of the 
extensors, and clawhand in paralysis of the interossei, but in most 
cases of this disease the foot is the part involved in the disorder. In 
progressive muscular atrophy the atrophy often precedes the par- 
alysis, whereas in poliomyelitis the paralysis precedes the atrophy, 
so that in the former the reaction of degeneration develops late, and 
in the latter develops early. 

A somewhat claw-shaped hand is also sometimes seen in that very 
rare condition called Morvan's disease, but it has not the character- 
istic appearance of main-en-griff e, there being a slow symmetrical 
wasting of the muscles with a drawing of the fingers into flexion. 



44 



THE HANDS AND ARMS 




There are also analgesia and painless whitlows. It usually occurs 
in young and middle-aged males. Morvan's disease of the fingers, 
as already stated, may arise from a syringomyelia and neuritis, or 
neuritis alone. 

Another spinal lesion producing great alterations in the appearance 
of the hand and arm, through wasting of the thenar and antithenar 
and interossei and the muscles of the arm, is amyotrophic lateral 
sclerosis. Here again the hand often shows the first manifestations 
of the disease in the loss of power of which the patient complains. 
The early symptoms of amyotrophic lateral sclerosis may closely 
resemble those of progressive muscular atrophy in the loss of power 

in the thumb muscles, but in this 
disease the reflexes are markedly 
increased in the affected muscles, 
whereas in progressive muscular atro- 
phy they are lost, although fibril- 
lary muscular twitchings may be 
caused by tapping. Again, the patient 
is usually manifesting some of the 
symptoms of lateral sclerosis when he 
comes before the physician, such as 
weariness, stiffness, and loss of power 
in the legs. (See chapter on the Legs, 
Paraplegia.) There are also exag- 
gerated knee-jerks and ankle clonus, 
and wrist-jerk is marked. 

Wasting of the muscles of the 
hand, causing distortion, may also be 
due to syringomyelia, but generally 
there will be, with this, loss of power 
and disturbance of sensation, such an 
anesthesia. Often in syringomyelia 
there will be developed an arthrop- 
athy of the arms such as is seen in 
the legs in tabes. 
Wasting of the hand, with flexion and rigidity and sometimes 
contractures, is seen rarely in advanced paralysis agitans in place 
of the characteristic tremor. 

In the "cerebral palsy of children" sometimes called "spastic 
infantile hemiplegia," the hand may be flexed on the forearm, and 
the forearm on the arm, the thumb drawn into the palm of the hand 
and the fingers flexed as in Fig. 14. These deformities are not neces- 
sarily confined to one arm alone, but are sometimes bilateral. A 
peculiarity of these cases is that the muscles waste very slightly, and 
do not develop the reactions of degeneration, so that the case sepa- 




Fici. 14. — Right hemiplegia, with con- 
tractures and retarded growth of arm . 
Onset of disease at eight years of age, 
following typhomalarial fever. (Sachs.) 



INSPECTION OF THE HANDS 45 

rates itself from poliomyelitis. The fingers in the cerebral palsy of 
children can often be placed in curious positions with ease, and, if 
the limb be suddenly flexed, a lock-like sensation will be imparted 
to the physician's hand. Convulsive seizures of an epileptiform 
type are very frequent in cases of cerebral palsy in children. Cohn 
asserts that there are on record eight cases in which intention tremor 
has taken the place of the spastic rigidity just described, and he 
reports a ninth. Similar lesions may follow infantile cerebral 
hemorrhage, thrombosis, or embolism. 

Again, in persons who have had apoplexy it is not uncommon as 
time goes on for the temporary spasm seen in the muscles of the haul 
and arm to be replaced by permanent contractions resulting in 
deformity. These contractions, if they occur early, are an evidence 
of irritation of the pyramidal tract or the fibers just behind the knee 
of the internal capsule, and are of serious import, as they indicate 
the extension of marked inflammatory processes. When they come 
on later they show that a degenerative process is descending the 
pyramidal tracts. Wasting finally comes on. (For further discus- 
sion of the significance of paralysis in the arm and hand, see suc- 
ceeding pages and chapter on Hemiplegia.) 

A very important point always to be remembered in examining 
contractures of the hand and arm, or of the lower limbs, is the fact 
that they often are due to hysteria, in which case the history is that 
they set in suddenly, and they are generally accompanied by other 
hysterical manifestations, which can be discovered if sought for. 
As a rule, the muscles do not waste or develop degenerative reac- 
tions, but rarely such wasting may occur. Care must be taken in 
giving a prognosis for cases of hysterical contracture, since organic 
lesions sometimes supervene. Charcot states that if the contractures 
persist when the patient is under anesthesia, and the muscles arc 
atrophied, organic disease exists. It is important to remember this, 
for these contractions may be practically permanent when once 
induced, and, as injuries may produce either a true organic or a 
false hysterical contracture, much medicolegal interest centres about 
this differential diagnosis. Closely allied to these cases are those of 
hysterical contracture, in which after grasping an object the patient 
cannot let go until the muscles are stroked. Putting an Esmarch 
bandage on such a forearm will usually produce the spasm. 

When in the course of an acute illness in a child the fingers are 
drawn down into the palm of the hand, with the tips touching the 
palm and the thumb turned in beneath them, with its tip pressing 
the palm, the patient may have meningeal congestion or inflamma- 
tion, or hydrocephalus, and a general convulsion may be imminent. 

When the fingers are bent toward the palm, but the tips extended 
and the thumb turned in ("the accoucheur's hand"), the position 



46 THE HANDS AND ARMS 

is typical of tetany, but in this condition the rest of the body will give 
evidence of involvement. The nervous irritability in this condition 
is greatly increased, and pressure on a large bloodvessel or nerve 
trunk will often produce the spasm. Curiously enough, gastric 
dilatation or thyroid wasting will often be found with tetany. In 
other cases it appears to be due to profound debility, as after pro- 
longed nursing. (See Tetany in chapter on Convulsions and General 
Spasms.) Care must be taken to separate the so-called carpopedal 
spasm of rickety, hydrocephaloid children rom true tetany, in 
which the body is usually involved, and from spastic paralysis due 
to infantile cerebral palsy. 

Spastic rigidity of the arms is often one of the earliest signs of 
chronic hydrocephalus, even before the skull begins to enlarge, and 
convulsions may be present from time to time. In congenital spastic 
rigidity due to sclerosis or defective development of the cortex 
cerebri the spastic condition is usually confined to the legs. (See 
chapter on the Legs and Feet.) 

Spasm of the fingers of a rigid type on attempting to make cer- 
tain movements is also seen as the result of excessive use of the 
part involved, and occurs in seamstresses, cigarette rollers, cigar 
rollers, typewriters (rarely), telegraphers, milkers (rarely), persons 
who use a pen to excess, and in piano, flute, clarionet, and violin 
players, or in persons engaged in any occupation requiring constant 
and comparatively minute and well coordinated effort. It seems 
to be more common in men than in women by a large proportion 
(39 to 4). Sometimes paralysis, tremor, or vasomotor disturbances 
take the place of occupation spasm. 

The spasm resulting from occupation must be separated from that 
sometimes seen in the hand in posthemiplegic chorea, progressive 
muscular atrophy, the various forms of toxic peripheral neuritis, 
and that due to irritative cerebral foci, such as tumors of the brain. 
The history nearly always clears up the diagnosis. Spasm of the 
muscles of the hand and arm, rhythmical or otherwise, may also 
be due to hysteria, and may resemble when due to this cause, true 
tetany (not tetanus). 

The position of the hand may be very various. Thus, the hand 
may drop edgewise from the radius toward the ulna in cases of 
rheumatoid arthritis, from paralysis of the extensors on the radial 
side of the forearm, resulting from neuritis or acute infantile polio- 
myelitis, while marked wrist-drop may occur from paralysis of 
the extensors in chronic lead poisoning, or in any form of neuritis, 
toxic or otherwise, involving the nerve supply of these muscles 
(musculospiral nerve). Wrist-drop may also be developed by 
pressure upon the musculospiral nerve, as in crutch palsy. If 
the wrist-drop is bilateral, it may be due to toxic neuritis; but if 



INSPECTION OF Till-: HANDS 47 

unilateral, it is probably, but not positively, due to pressure paralysis 
from sleeping with the head resting on that arm, or from pressure 
by a crutch, or from some similar pressure capable of injuring the 
nerve. Very rarely unilateral wrist-drop is seen in lead poisoning. 
When lead is the cause, the supinator longus usually escapes, as 
does also the short extensor of the thumb, so that the forearm can 
be flexed and the thumb extended. Pain is rarely present in pres- 
sure or lead wrist-drop, but is present in wrist-drop due to alcoholic 
and other forms of toxic neuritis. Often, too, in these cases the 
flexors are considerably involved. (See part of this chapter on 
Brachial Monoplegia.) 

Choreic movements of the hands and arms in children are seen 
chiefly as a manifestation of chorea minor. They are usually met 
with in rheumatic and neurotic children, and heart murmurs are 
generally to be heard in these cases. The first evidences of spasm 
may be developed in the hand, and be limited to that member in 
rare cases, and the hand often drops things that are placed in it. 
The hand itself is rarely involved alone, and the muscles of the arm 
toss the entire arm and hand with a fidgety, jerking movement which 
is very characteristic. A form of chorea minor, usually limited to the 
arm, is called paralytic chorea. It comes on suddenly, and is charac- 
terized by loss of power with a few feeble twitches. It affects only 
children. The same term, "paralytic chorea," is also applied to a 
condition sometimes seen after an apoplectic stroke, choreic move- 
ments taking place as degenerative changes in the muscles are 
developed. Sometimes choreic movements come on in the latter half 
of life, often preceded by emotional disturbances. These move- 
ments are not true chorea. They are often called senile chorea. 

In some cases of adult chorea the patient tends to become mania- 
cal, particularly toward night. Such cases usually occur in women, 
and the prognosis as to life is bad. There is often in these cases 
great mental hebetude. 

Several other affections which somewhat resemble true chorea are 
sometimes met with, but all of them lack, with one exception, the 
peculiarity of its movements. One of these is what has been called 
habit chorea, or, more correctly, habit spasm, in which condition 
the patient acquires a nervous trick of jerking a muscle or a set of 
muscles. Unlike true chorea, it is more frequently seen in adults 
than children. Its limitation, as a rule, to a single set of muscles 
and the history of the case usually separate it from chorea minor, 
and it is to be recalled that the movements consist in sudden twitch- 
ings rather than jerking, irregular muscular movements. 

In paramyoclonus multiplex the disease, as the name implies, 
usually involves symmetrical parts, the contractions of the muscles 
appear in paroxysms, and the muscles involved are usually the biceps, 



48 THE HANDS AND ARMS 

deltoid, and triceps in the arms, and the quadriceps femoris and calf 
muscles of the lower limbs. Myoclonus multiplex is a disease of 
adult life, and chorea is usually seen in childhood. Sometimes 
the muscles in myoclonus are exceedingly irritable. 

Under the name of electric chorea, or "Dubini's disease," Dubini 
described a disease, affecting both sexes and all ages, in which sud- 
den shock-like contractions of the muscles take place, as if they 
were being stimulated by a slowly interrupted faradic current. 
The disease usually begins in the upper extremities, and gradually 
involves the rest of the body, and progressively passes to a fatal 
issue. This is a very rare disease, and the sudden contraction of 
the muscles in tonic spasm separates it from chorea. 

Still another form of electric chorea is that of Bergeron, which is 
probably identical with what has been called hysterical chorea. 
Here, again, the shock-like muscular contractions are manifested 
chiefly about the shoulders. The patient is usually a female, and 
has the stigmata, sensory and otherwise, of hysteria. (See chapters 
on the Skin, Eye, and Feet and Legs.) 

Again, the physician may meet, exceedingly rarely (almost never 
in the United States or England), with a condition called convul- 
sive tic or palmus, which has also been called "the jumpers," in 
which the movements are not in the slightest degree like true chorea, 
but are sudden muscular movements, usually imitative of the act of 
some other person or animal. This is often associated with echolalia 
— that is, repeated or echoed speech — or coprolalia or filthy speech. 

Finally, another very rare disease is that known as Huntingdon's 
or hereditary chorea, a condition in which the twitching usually 
begins in the face and extends to the arms and legs. This ailment 
is hereditary, rarely begins before thirty years of age, is accom- 
panied by progressive mental deterioration, a tendency to melan- 
cholia, and may last ten or twenty years. 

Mercurial poisoning producing tremor may cause so coarse a 
movement in advanced cases that the case may be thought choreic. 
(For a description of tremors, see latter part of this chapter.) 

In " Thomsen's disease" the hand is placed in tonic spasm as 
soon as voluntary movement is attempted. Closely resembling 
Thomsen's disease, or myotonia congenita, is what is called para- 
myotonia congenita, which exists in three forms: first, a patient 
suffering from paralysis agitans on attempting to move is seized with 
rigidity of the muscles, which holds him fixed; second, a patient is 
suffering from ataxia and muscular weakness, and is seized with an 
attack of muscular rigidity; and, third, a patient may have the mus- 
cular fixation occurring just as it does in Thomsen's disease, save 
that it is produced by cold or exposure, and not by intention move- 
ment, and may last for hours. (See also Athetosis.) 



TREMORS OF THE HAM) AND ARM 49 

Tremors of the Hand and Arm. — The movements of the hand should 
always be carefully watched in cases of suspected nervous disease. 
The most common alteration from the normal will be found to be 
tremor, which may indicate paralysis agitans, disseminated sclerosis, 
general paresis, chronic mercurial, plumbic, or alcoholic poisoning, 
hysteria, senility, and Graves' disease. Sometimes a tremor may be 
found in naturally nervous women who are drinkers of tea to excess. 

In paralysis agitans the whole hand is involved, and generally 
both hands are equally affected. The tremor is rhythmical and fine 
or minute in character at first, but later may be quite coarse. It is 
a slow tremor of about five vibrations per second, which is more or 
less constant, and worse when attention is called to it, but it is not 
greatly increased, and, perhaps, is even decreased, by a voluntary 
act, such as an attempt to raise a glass of water. Very rarely, 
however, the reverse holds true, and the tremor is increased In- 
voluntary effort. The fingers are generally semi-extended and the 
thumb is adducted, so that it constantly rubs the index finger with 
its pulp, as if it were attempting to rub off the skin of that member. 
Frequently there are pain and aching of the extensor muscles of 
the forearm and wrist from the constant exertion. (See chapter 
on the Feet and Legs, the part on Gait. ) 

The tremors of disseminated sclerosis arc also slow, but coarse in 
character. They are not constant, but are developed upon inten- 
tional movement, and have a greater amplitude than those of Park- 
inson's disease paralysis agitans). Indeed, they may be so coarse 
as to be choreic in type or even ataxic. Often threading a needle 
will be possible for a person with this disease, because it is a short 
act, while lifting a glass of water will be impossible. The symp- 
toms of disseminated sclerosis are well summarized in the follow- 
ing table drawn up by Charcot. 

I. Spinal Symptoms : 

f Tremor on voluntary movements of the extremities— "intentioD 
tremor" (arms and head ; more rarely of legs). 
Positive . . . . \ Titubation. 

| Paresis (spasmodic) of the extremities. 

[ Contracture, with exaggeration of the reflexes— spastic rigidity. 



Negative . . . . J 
II. Cerebral Symptoms 



No sensory symptoms, or only very slight disturbance. 
Vesical disturbance none or very slight. 



Dysarthria — slowness of speech ; scanning of words. 

Nystagmus— blank expression. 

Attacks of vertigo — spasmodic myosis. 

Transitory amblyopia— white atrophy of the papilla. 

Diplopia— associated paralysis of ocular muscles. 

Mental enfeeblement. 

Apoplectiform and epileptiform attacks. 

Difficulty in deglutition. 



50 THE HANDS AND ARMS 

III. Abnormal or Unusual Symptoms : 

Trophic Muscular atrophies (amyotrophies), bedsores, 

f Lightning pains. 

| Romberg symptom. 
Tabetic -j Anaesthetic areas. 

j Vesical and rectal paresis. 

[ Gastric crises. 

Frequent remission of all the symptoms is characteristic of the malady. 

It is not to be expected that all these symptoms will be found 
in one case. But many of them will occur. Charcot taught that 
tremor involving the head indicated disseminated sclerosis, and 
excluded paralysis agitans; but cases of head tremor in the latter 
disease do occur. (See chapter on the Feet and Legs, part on Gait.) 

The tremor of mercurial, plumbic, and alcoholic poisoning resem- 
bles that of paralysis agitans, save that it is more rapid, reaching 
nine or ten vibrations per second, and in the case of alcoholic tremor 
is decreased by a large drink of liquor, while those due to lead and 
mercury may be relieved in a short time by potassium iodide. 
Further than this, the tremor of alcoholism is generally worse in 
the morning. 

A point of some importance in plumbic neuritis producing tremor 
and wrist-drop is the fact that painful sensations are rarely present; 
in arsenical neuritis, on the other hand, they are often the most 
prominent symptoms, even preceding the motor disturbance. In 
mercurial neuritis, on the other hand, tremor precedes all evidence 
of loss of power, and, finally, may become so coarse as to resemble 
chorea. 

The tremor of general paresis is also rapid, eight or nine per 
second, and is a very fine tremor, which may be felt only when 
the arm is extended and the finger rested on the hand of the physi- 
cian. In other words, the tremor of the hand in general paresis is 
generally not a predominant symptom, but is elicited when the 
muscles are put upon a strain. In regard to the fineness of the 
tremor of general paresis, it should be remembered that it closely 
resembles that of Basedow's or Graves' disease (exophthalmic 
goitre, eight or nine per second), since the tremor of this condition 
is not only equally fine, but generally unseen except when the arm 
is extended and tips of the fingers rested upon the fingers of the 
doctor. This tremor has been called the "railroad-bridge tremor," 
because of its fineness and vibratory character. The individual 
fingers do not separately tremble in Graves' disease. 

In posthemiplegic tremor the trouble is unilateral, there is a 
history of cerebral disease, and paralysis is present. 

Tremor of a very marked character may be due to hysteria, and 
arises most frequently in those who have been exposed to shocks or 
accidents. The tremors may occur constantly or only with inten- 



GENERAL MOVEMENTS OF THE HAND AND ARMS 51 

tion movements, or be increased in amplitude, but not in rhythm on 
movement. The latter form is known as the "type Rendu," and 
has a rhythm of seven to nine per second, while the slower hysterical 
tremor may be four or five per second. 

Beyond the state of tremor should be recalled the movements of 
chorea, which may be limited to one arm or hand, and which in their 
milder forms may be confused with the pronounced movements 
produced by effort in disseminated sclerosis. The latter arc 
often very arhythmical, and so the choreic movement the more 
closely resembles them; but those of sclerosis are purposive, while 
those of chorea are not, since the movement contemplated in chorea 
is opposed by a contradictory contraction. 

General Movements of the Hand and Arms. — Aside from the move- 
ments of tremor, careful notes should be made of the movements 
of the hand as a whole, of the coordination of its fingers and of the 
arm governing it. Thus, trembling contractions of the extensor 
tendons (subsultus tendinum) are a sign of grave and advanced 
forms of typhoid fever, and picking at the bedclothes (carphologia) 
is of still graver import. (See beginning of this chapter.) Inability to 
write, to play musical instruments requiring the use of the fingers, 
or to sew, may indicate the rare form of locomotor ataxia involving 
the upper extremities, so that if the patient is asked to close his eyes 
and feed himself the fork or spoon misses his mouth through lack 
of coordination, although loss of power may not be present. 

Sometimes in locomotor ataxia as the disease becomes advanced 
paroxysmal twitching of the fingers may come on, or involuntary 
movements of the fingers occur in association with voluntary move- 
ments elsewhere. 

In locomotor and Friedreich's ataxia also the movements of the 
hand are often lacking in coordination. The hand may be advanced 
past the object which the patient desires to grasp, or else falls short 
of it. On endeavoring to pick up an object the fingers are spread 
over it like a widespread claw. Generally these ataxic symptoms 
will be more marked in the other parts of the body and be bilateral, 
but Ormerod has reported an instance in which only one hand (the 
left) was involved. This faulty movement of the hand may, how- 
ever, be due to the fact that the ocular muscles are affected, and the 
"erroneous projection" due to this cause leads the patient to pass 
the hand beyond the object reached for. Overdoses of strychnine 
sometimes cause this symptom of "erroneous projection." 

When fibrillary twitchings of the muscles occur and tapping 
the muscles produces idiopathic muscular contraction, progressive 
muscular atrophy may be present or profound asthenia. 

Sometimes, as the result of infantile cerebral paralysis or from 
lesions developing in later life, the muscles of the hand are affected 



52 THE HANDS AND ARMS 

by a slow, constant movement, so that the fingers assume curious, 
constrained, and unusual postures, being moved into extreme or 
forced extension, flexion or pronation, or supination. This con- 
dition is called athetosis, and is separable from chorea in that the 
movements are slower and limited to the fingers and wrists, the 
arm escaping. 

Very rarely athetoid movements of the fingers occur in advanced 
spinal tabes (locomotor ataxia), probably as the result of a related 
lesion, and not from tabes itself. 

In this connection mention should be made of " mirror writing," 
a curious condition in which the patient writes from right to left 
instead of left to right. It occurs in some cases of mental feeble- 
ness, hereditary or acquired, and rarely in hysteria. " Mirror 
writing" may also be present in cases of cerebral paralysis. 

Paralysis of One Arm, or Brachial Monoplegia. — Absolute loss of 
power in one hand and arm without the necessary development of 
subsequent deformity results from cerebral or peripheral lesions, 
as a rule, being rarely spinal in origin, and is called brachial mono- 
plegia. The causes of this loss of power when its origin is cerebral 
may be various. Thus, the lesion may be cortical or subcortical; 
that is, in the surface of the brain or in the internal capsule, or 
between the cortex and the capsule in the corona radiata. As a 
rule, however, monoplegia is cortical in origin, for below the cortex 
the motor fibers run so closely together that only a very small lesion 
can involve one without involving all, and so producing a hemiplegia. 
These cortical lesions when they do occur are generally, but not 
always, associated with a convulsive seizure in the paralyzed limb, 
and Seguin has called this convulsion the "signal symptom" indi- 
cating a cortical lesion. Brachial monoplegia not due to hysteria 
or neuritis, preceded and accompanied by a convulsion and loss 
of consciousness, and lacking in signs of involvement of lower 
nervous centres, is, therefore, cortical, and is generally due to the 
formation of a clot in the hand and arm centre resulting from injury 
or from the ordinary vascular causes of apoplexy. In other cases 
it is due to cerebral embolism or thrombosis, or to the growth of 
some neoplasm, specific or otherwise, or to a localized meningitis. 

The probability of the lesion being an embolism or thrombosis is 
decreased by the recollection of the fact that the cortex is so well 
supplied by vessels from the pia mater that paralysis of a centre 
from lack of blood supply from such a cause is rare, unless the 
lesion is subcortical, or, in other words, not deep enough to involve 
fibers from other centres as they approach each other, and yet suffi- 
ciently deep to prevent the tissues from partaking of the nutrient 
blood supply from the pia mater as just mentioned. Aside from 
the discovery of a condition of the internal organs, such as cardiac 



PARALYSIS OF ONE ARM 53 

valvular disease or sepsis, whieh might cause embolism, the diag- 
nosis between paralysis from hemorrhage and embolism is prac- 
tically impossible, and this is also true of the paralysis due to throm- 
bosis, except that in cases of thrombosis we often find the presence 
of general endarteritis or an infectious disease, and the paralysis of 
thrombosis may be slow and gradual in its onset. If the paralysis 
rapidly spreads, the lesion is probably due to a hemorrhage. 

The history of there having been some sudden cause for an 
increase in arterial tension, as by muscular effort, and the presence 
of atheromatous vessels aid us in deciding as to the probability of 
the lesion being due to a hemorrhage, and the sudden onset, coupled 
with the symptoms named, makes the diagnosis clear in a certain 
proportion of cases. 

Neoplasms or tumors of the brain producing monoplegia are 
gradual in their development, accompanied generally by headache, 
by changes in the optic disks, and sometimes by mental disturbances 
or pressure symptoms. A specific history pointing to the formation 
of a syphilitic tumor is of value in the diagnosis. (See chapter on 
Headache.) 

If brachial monoplegia results from a lesion in the internal cap- 
sule, the lesion must be very limited, or, in other words, only large 
enough to cut off the hand and arm libers. Tumors and lesions 
from traumatisms in this area are very rare, and hemorrhages, which 
frequently cause paralysis by affecting this area, are generally pro- 
fuse enough to cause hemiplegia — that is, injury of the motor fibers 
supplying the leg muscles as well. Sometimes, however, a sudden 
inflammatory process is set up in the tissues surrounding a tumor, 
and this may precipitate sudden paralysis. 

Although the onset of a monoplegia due to cortical, subcortical, 
or capsular causes is sudden, the reactions of degeneration do not 
come on for a long period of time in such cases, because the muscles 
in the paralyzed area are still connected with the trophic centres in 
the cord, and this affords us a valuable point in differential diagnosis. 

Sometimes a suddenly developed monoplegia affecting the arm 
comes on as a manifestation of hysteria, and follows the type of true 
cerebral hemorrhage so closely as to almost defy diagnosis. This 
condition may be accompanied by hysterical edema, the hand becom- 
ing puffy and swollen. The presence of a neurotic temperament 
and other hysterical signs, coupled with the prompt development of 
contractures, and the fact that the muscles do not rapidly waste, 
point to the cause of the loss of power in some cases, and this is 
emphasized if the presence of hysterical anesthesia of the skin can 
be discovered. Further, if the hand is affected, Patrick asserts 
that in making an attempt to grasp an object the thumb and fore- 
finger are chiefly used; but if the object is placed suddenly in the 



54 THE HANDS AND ARMS 

ulnar part of the hand, the remaining fingers can grasp it easily. 
(See chapter on the Skin for additional hysterical symptoms.) 

Brachial monoplegia is very often the result of injury to the 
brachial plexus or to some of its important branches. The symp- 
toms consist in heaviness or numbness of the arm with more or less 
loss of power. The motions of the arm which are particularly 
affected are usually abduction and elevation, which movements 
depend upon the circumflex nerve. If the power of extending the 
arm is lost, the loss depends upon paralysis of the musculospiral, 
which supplies the triceps; whereas if the power to flex the forearm 
is lost, there is paralysis of the musculocutaneous, which is the 
supply of the brachialis anticus and biceps. If the supinator longus 
is involved, the musculospiral is also affected. 

When brachial monoplegia depends for its existence upon primary 
brachial neuritis there is pain in the wrist and hand at first, or on 
the scapula and in the axilla, thence radiating down the arm. This 
pain is constant and dull, and now and then excruciating, and 
is made worse by movement, even when the loss of power is com- 
paratively slight. Sometimes, on the other hand, when the neuritis 
is septic in origin, it may start in the ulnar nerve and gradually 
extend up to the plexus. In still other cases brachial monoplegia 
may depend upon fracture or dislocation of the head of the humerus, 
and in such a case the paralytic symptoms are apt to be very well 
developed. The musculospiral nerve is often paralyzed by fracture 
of the humerus, and this results in paralysis of the muscles of the 
back of the arm and forearm and back of the hand, and loss of 
sensation in the skin covering these parts. 

In all cases of brachial monoplegia due to peripheral lesions, as in 
severe neuritis, we find that atrophy of the muscles comes on very 
rapidly owing to the cutting off of the muscles from their trophic 
centres in the spinal cord. 

Sometimes in locomotor ataxia the peripheral nerves seem quite 
as much involved as the spinal cord, and symptoms precisely like 
the paralysis of a toxic neuritis develop. Thus, Strumpell has re- 
ported cases of musculospiral paralysis from this cause, and Remak 
and Hirt record cases in which the median nerve has been affected, 
so that not only loss of power but wasting of the muscles has re- 
sulted. This is particularly the case if the muscles are much used 
in daily pursuits. The ulnar nerve may also be affected. Such cases 
are separated from pseudotabes, due to neuritis, by the pupillary 
reflexes and other pathognomonic ataxic symptoms. (See chapter 
on the Feet and Legs and that on the Eye.) Widespread muscular 
atrophy of the arm sometimes takes place in locomotor ataxia as 
a result of a coincident neuritis. 

There are still to be considered two comparatively rare forms of 



PARALYSIS OF ONE ARM 55 

brachial monoplegia of the plexus type, namely, that due to 
pressure of growths in the neck or axilla, and brachial paralysis of 
the upper arm type, sometimes called Erb's paralysis. This latter 
form occurs from paralysis of the fifth and sixth cervical nerves 
or their roots. In adults this commonly results from blows or heavy 
weights striking on the shoulder, and in infants from pulling on 
the neck in difficult labor. As already said, it is an upper arm 
palsy, and is due to the loss of nerve supply to the deltoid, biceps, 
brachialis anticus, and supinator longus and brevis, and the supra- 
and infraspinatus muscles. The adult form is often associated with 
anesthesia and is persistent. In infants it is often temporary, and 
sensory symptoms are commonly absent. 

When the lower arm is paralyzed as the result of trouble in the 
brachial plexus, the lesion is in the nerves arising from the seventh 
and eighth cervical and first dorsal roots, and the muscles affected 
are the triceps, the flexors of the wrist and fingers, the pronators of 
the hand, the extensors of the fingers, and the muscles of the hand. 
The arm can still be raised by the deltoid and the forearm flexed on 
the arm by the biceps. 

When there is wasting with paralysis of the thenar, hypothenar, 
and interossei muscles, not due to progressive muscular atrophy, 
with anesthesia in the arm and forearm in the part supplied by the 
ulnar nerve, and in addition myosis on the side of the lesion, with 
sluggish pupil, retraction of the eyeball, and partial closure of the 
lids, there is probably a lesion of the first dorsal root of the brachial 
plexus and the communicating branch of the second dorsal. The 
cause may be neuritis or pressure by a tumor. This form is some- 
times called "Klumpke's paralysis." 

(For a description of the areas involved in the spinal cord, which 
cause loss of power in the arms and legs, see chapter on Feet and 
Legs, part on Paraplegia, and tables of localization in that chapter, 
also plates in chapter on Skin.) 

The presence of bilateral brachial monoplegia should always 
make the physician suspicious of lead poisoning or crutch paralysis. 

Apparent brachial monoplegia, in reality a syphilitic pseudo- 
palsy, has been described particularly by Parrot. A child appar- 
ently perfectly well, and but a few weeks old, suddenly loses the 
power of its arm, so that the member hangs like a flail. No wasting 
takes place, no degenerative reactions occur, but there may be some 
pain and crepitation on moving the arm. The cause of these symp- 
toms lies in the fact that there has been a separation of the epiphyses 
from the shafts of the bones, with consequent helplessness. Some- 
times general paralysis of the extremities arises from the extension 
of the disease to other limbs. The prognosis as to life is bad. 

It yet remains for us to discuss the paralysis of several important 



56 THE HANDS AND ARMS 

groups of the muscles of the arm. If the forearm cannot be flexed, 
there is loss of power in the biceps and brachialis anticus, and to 
some extent in the supinator longus; and as the first two muscles 
are supplied by the musculocutaneous, and the third by the musculo- 
spiral, such a failure in flexion shows paralysis of these fibers. 

Paralysis of the extensors of the forearm, wrist, and hand, and 
of extension of the elbow, with wrist-drop in consequence, and 
flexion of the tips of the fingers, is due to disease affecting the 
musculospiral nerve, but the fingers can still be partly extended 
through the action of the interossei and lumbricales, provided the 
tips are flexed. The back of the hand and wrist become unduly 
prominent after a short time because of the forced flexion of the 
hand and rapid wasting of the extensors. In most cases the supi- 
nator longus, which supinates the forearm after it is pronated, is 
paralyzed. When the ability to pronate the forearm is greatly 




Fig. 15. — Dynamometer. 

impaired, and the thumb is extended and abducted, so that it cannot 
be brought in contact with the tips of the fingers, the trouble is 
probably paralysis of the median nerve, and this is confirmed if all 
the phalanges are paralyzed except the first. 

If the arm cannot be moved outward, away from the body, there 
is paralysis of the deltoid supplied by the circumflex nerve. In 
this connection attention should be called to the loss of power with 
wasting of the muscles seen after direct blows on the muscle or after 
injuries to the joint, sometimes called " joint palsies." 

Brachial Paresthesia. — Disturbances of sensation in the hand and 
arm consist in anesthesia, analgesia and numbness, tingling and 
pain. The area of these sensations depends upon the nerve trunks 
involved, and to some extent upon the degree of involvement. 
Thus, if the function of the nerve is merely impaired, the sensation 
may be that of tingling or pain; if still further impaired, the sen- 



PARALYSIS OF ONE ARM 



57 




Fig. 16. — Testing the elbow, or biceps, jerk. 




Fig. 17. — Testing the elbow, or triceps, jerk. 



58 THE HANDS AND ARMS 

sation may be that of numbness; and if the sensory fibers be totally 
destroyed or paralyzed, absolute anesthesia and analgesia may be 
present. (See Anesthesia, chapter on the Skin.) 

Physical Methods Employed in Examining the Hand and Arm. 
The Dynamometer. — The use of the dynamometer is to determine 
whether there is a marked difference in the strength of the flexor 
muscles in either forearm. The dynamometer most commonly 
used is that of Mathieu, which is an elliptical spring surrounding a 
semicircular scale over which moves an indicator according to the 
flattening of the ellipse produced by pressure. (See Fig. 15.) 

The Elbow- jerk. — This is produced by striking the tendon of the 
triceps or the biceps, the forearm being somewhat flexed on the arm, 
and supported by an assistant or by the physician himself. (See 
Figs. 16 and 17.) (For methods of testing the various forms of 
sensibility in a limb, see chapter on the Skin.) 



CHAPTER III. 

THE FEET AND LEGS. 

The general appearance of the feet and legs when clothed — The gait — Spastic 
paraplegia — Paraplegia without spastic contraction — Crural monoplegia — 
Deformities of the feet and legs — The jomts — Alterations in the nutrition 
of the feet and legs aside from a change in the muscles. 

As the physician sees a patient approaching him, he can often 
gain information as to the ailment from which the man is suffering 
by noticing his gait and the appearance of the legs and feet, for, 
while the gait varies greatly in normal individuals, in some diseases 
it is so typical that he who runs may read the diagnosis. A glance 
at the feet revealing one foot more loosely covered than the other, 
or a slit in the shoe, or a very loose lacing, will point to the pres- 
ence of some inflammatory or dropsical swelling, which forces the 
patient to give it room; and if the legs of a man of ordinary build 
look swollen and fill the trousers tightly, while a glance at his face 
reveals that it is puffy, rather than one which is obese, dropsy still 
more widespread is probably the cause. 

Gait. — Aside from local injuries causing a lame gait, we find that 
gout, rheumatism, and sciatica are the common causes of a limping 
gait, arising from trouble in one leg, and that in such cases there is 
a pained expression of the face at each movement, which shows the 
suffering that walking causes. The gait of such a patient is slow 
and cautious, and he is apt to rest every few steps, bearing his weight 
at such times chiefly on the well leg, or, by means of his hands, upon 
chairs or tables that may be near. Aside from the alterations of gait 
produced by these causes, we see very typical gaits produced by 
locomotor ataxia, pseudolocomotor ataxia (peripheral neuritis) due 
to alcoholic or lead poisoning, syphilis, or peripheral neuritis arising 
from other causes, Friedreich's ataxia, general paresis, chronic 
myelitis, lateral sclerosis, acute poliomyelitis, pseudomuscular hyper- 
trophy, cerebral infantile palsy, multiple sclerosis, paralysis agitans, 
cerebellar disease, organic and hysterical hemiplegia, and osteo- 
malacia, and the gaits caused by rickets and other bony defects. 

In Locomotor Ataxia the gait is unsteady and waveringly uncer- 
tain, resembling that of a blindfolded person who is told that he is 
approaching some inequality in the floor. The patient continually 
seems to be feeling for the ground with his feet, and carefully picks 
his way along a perfectly smooth surface in a labored fashion, using 



60 THE FEET AND LEGS 

a cane to help him both in the way of support and of feeling the 
ground. If he looks up from the ground while walking, he sways 
suddenly and may fall; and if prevented from returning his eyes 
to the pavement, almost surely falls if no aid is given him. 

The gait of pseudotabes is sometimes identical with that just 
described, is usually associated with a history of alcoholic excess, 
and is due to multiple neuritis. In a majority of the cases, how- 
ever, it is distinctive, and has been called the "steppage'' gait. 
The foot is thrown forward and the toe is raised so that the heel 
first strikes the ground in much the manner adopted when one 
attempts to step over some obstacle. Sometimes this gait is found 
in cases of arsenical neuritis and that due to lead, but in alcoholic 
tabes there are generally mental symptoms associated with this gait, 
while in lead poisoning the pathognomonic signs of this condition, 
such as the blue line on the gums and wrist-drop, when combined 
with the history, clear up the diagnosis. It must not be forgotten, 
however, that the differential diagnosis of tabes from pseudotabes 
is sometimes very difficult, and as Dana has well said: "When 
Dejerine described as locomotor ataxia a case which now appears to 
have been one of alcoholic peripheral neurotabes, when Buzzard has 
diagnosticated as true spinal tabes a case of postdiphtheritic ataxia, 
when Seligmueller mistakes a case of wall-paper poisoning for one 
of true spinal tabes, we may easily suppose that errors have been 
made by many others." 

The important symptoms which point to true locomotor ataxia 
are the swaying of the body when the eyes are closed (Romberg's 
symptom), the loss of knee-jerk (Westphal's sign), the history of 
gastric, laryngeal, or vesical crises, the presence of numbness in the 
feet, the slow onset of the disease, and the absence of any history of 
exposure to the causes of neuritis just named. Additional diagnostic 
points are the inability of the patient to stop and turn quickly and 
steadily at the command of the physician. 

Frankel states that in many cases of this disease the sensation of 
passive motion at the joints is impaired. To determine the presence 
of this symptom the toe is grasped by the thumb and forefinger, 
and moved very slowly and gently so as not to disturb the rest of 
the limb. The patient must be blindfolded, and in ataxia fails to 
appreciate that passive joint movement has been made. If all 
these signs are present, and are combined with that important 
symptom, the Argyll-Robertson pupil, the diagnosis is practically 
certain. 

Grube has, however, reported three cases of diabetes mellitus pro- 
ducing a pseudotabes due to neuritis which had the Argyll-Robertson 
pupil, and in addition attacks of abdominal pain like the crises of 
true ataxia. 



GMT 



61 



Another sign of locomotor ataxia is undue relaxation of the mus- 
cles, which has been called hypotonus. This is a point much insisted 
upon by Frankel. He points out that if a healthy man be placed 
in a horizontal position on a couch, he cannot raise the leg very high 
if the knees be kept extended. On the other hand, if he has 
locomotor ataxia, even with the knee fully extended, he can raise 
the leg to a sharp angle with the plane of the body, amounting to 
00°, 80°, or 100°; whereas in health he cannot raise it to an angle 
greater than 30° to 50°. This is due to the fact that the semi- 
membranosus and semitendinosus resist the movement in health; 
whereas in locomotor ataxia they are so relaxed that this resistance 
does not occur. Again, because of hypotonicity of the quadriceps, 
it may be possible in such patients to flex the knees to such an extent 
that the heel can readily touch the buttocks in voluntary motion. 
So, too, the thighs when the legs are flexed may be so widely abducted 
that the knees come in contact with the couch, because of relaxation 
of the abductors. 

The Stages of Tabes Dorsalis. 



Initial Period. 



Second Stage. 



Inco-ordination, but no change 
of gait. 

Numbness of the feet. 

Shooting-pains in the legs. 

Diminished or lost knee-jerks, 
one or both. 

Sluggish or lost pupillary reflex 
to light. 



Greater inco-ordination, and 
marked ataxic gait. 

More marked anaesthesias. 

Pains worse. 

Lost knee-jerks. 



Lost pupillary reflex to light 
and myosis. 



Final Station. 



Weakness of sexual function. Impotence. 



Transient diplopia ; transient 
ptosis 

Sluggish micturition. 

Optic atrophy. 

Trophic changes in the joints. 

Hemiatrophy of tongue. 



Ocular palsies rare, or marked 
ophthalmoplegia. 

Increased vesical weakness. 

Optic atrophy rarely develops. 

Trophic changes not so com- 
mon. 

' Deafness. 

Laryngeal and visceral crises. 

Girdle sensation. 



Cannot walk because of ataxia. 

Extensive anaesthesia. 
Pains less. 
Lost knee-jerks. 

Lost reflex to light, mynsis, 
paralysis of accommodation. 

Impotence. 

Ophthalmoplegia. 

Catheterization needed. 

Blindness. 

More marked if they began in 
early stage. 

Increased. 

Not so common. 

Unnoticed. 



Reflex action is decreased and the gait altered in locomotor ataxia, 
because, though the motor tracts are open, the sensory tracts in the 
nerves, the posterior nerve roots, and the posterior columns of the 
cord are diseased. (See Fig. IS.) For these reasons the reflex arc is 
destroyed and the coordination of the muscles lost. The patient 
cannot tell how to use his muscles unless he can see them and 



62 THE FEET AND LEGS 

coordinate them by the aid of the eye. The sensations of formication 
or numbness are also due to these sensory lesions. (For descrip- 
tions of motor and sensory tracts of the spinal cord, see early part 
of chapter on Hemiplegia and the chapter on the Skin.) 

In neuritis causing pseudotabes we have a history of rapid onset 
of the symptoms, paralysis, and wasting of the muscles, an absence 
of vesical symptoms and of the Argyll-Robertson pupils. 

Sometimes not only the gait, but the entire set of the ordinary 
symptoms of locomotor ataxia are aped by hysteria so closely that 



O 




Fig. 18. — Showing the areas of the cord involved in locomotor ataxia. 1. Primary lesion in 
sensory neurones in posterior ganglia. 2. Sensory nerve roots in which the earliest and most 
extensive lesions are found. 3 and 4. The shading includes both the column of Goll, the inner, 
and that of Burdach, the outer. 5. Also Clarke's column in the gray matter. It is to he 
remembered that the lesions of locomotor ataxia are found in the peripheral nerves as well. 

a diagnosis may be almost impossible, but the Argyll-Robertson 
pupil, the lost knee-jerks, and the optic atrophy will not be present 
if hysteria be the cause of the symptoms. On the other hand, 
Romberg's symptom may be marked to an extraordinary degree. 
The patient who is hysterical, in falling nearly always falls the 
same way, keeping her frame stiff like a board. (See chapter on 
Eye for differential ocular symptoms.) 



GAIT 



63 



General Paresis. — The feebleness of the limbs, the reflex irido- 
plegia (Argyll-Robertson pupil), and the ataxie gait sometimes seen 
as the chief manifestations of general paresis may cause an error 
in diagnosis in favor of locomotor ataxia, but careful examination 
will reveal mental feebleness in the paretic case, or at least evi- 
dences of delusions, and if the disease is at all advanced there will 
be a history of the patient having had convulsions or apoplectiform 
attacks. Sometimes there will be found present in paretic dementia 
(general paresis) increased knee-jerks and many of the symptoms of 
ataxic paraplegia, but the associated mental failure and fine intention 
tremor of the hands decide the diagnosis in favor of paretic dementia. 




Fig. 19. — Showing the spinal areas chiefly involved in Friedreich's ataxia. The areas are 
the column of Burdach (1); the lateral pyramidal tracts (2); the columns of Goll (3; the 
posterior nerve roots (1); the direct pyramidal tracts (5); atrophy of cells in anterior horn (6) 
and in the posterior horn (7); and the anterior nerve roots (8). 

In Friedreich's Ataxia the gait is peculiar. The legs are widely 
separated and moved in an uncertain, hesitating manner, and if the 
feet are placed close together and the patient is told to stand still, 
swaying at once develops. If the eyes be closed, the swaying may 
greatly increase. The movements of the arms are incoordinated. 
These symptoms, which to a certain extent simulate true locomotor 
ataxia, are associated, as a rule, with others which separate the two 
affections, for in this disease the symptoms often come on in very 
early life, there is sometimes nystagmus, usually a history of heredity 
there is a slow and jerky articulation, scoliosis, and talipes equino- 
varus, but there is no Argyll-Robertson pupil (Pig. 19). 



64 



THE FEET AND LEGS 



The following table shows the differential points between loco- 
motor ataxia and Friedreich's ataxia: 



Locomotor Ataxia. 
Argyll- Robertson pupils. 
No nystagmus. 
Painful crises. 
Intellect unimpaired. 
Gait ataxic. 
Speech normal. 
No head tremor. 



Friedreich's Ataxia. 
No Argyll-Robertson pupils. 
Present late in disease. 
Crises usually absent. 
Becomes impaired. 
Cerebellar ataxic gait. 
Speech halting. 
Head tremor present. 



Hereditary Cerebellar Ataxia. — Friedreich's ataxia must be separ- 
ated from another rare disease in which the gait is ataxic and the 
disease hereditary, namely, hereditary cerebellar ataxia, in which 
we have the following symptoms not seen in Friedreich's disease, 
namely, normal or exaggerated knee-jerks, Argyll-Robertson pupils, 
and a beginning of the malady after twenty years of age. 

Hereditary cerebellar ataxia may also be confused with dissemi- 
nated sclerosis. 



Hereditary Cerebellar Ataxia. 
1. Gait : ataxic, groggy ; feet wide apart. 



2. Station : Romberg's symptom absent. 

3. Arms : ataxy and some intention tremor. 

4. Oscillations and jerky movements of the 
head and trunk. 

5. Exaggerated contractions of facial mus- 
cles during speaking. 

6. Speech: hesitating and abrupt, or simply 
monotonous. 

7. Eyes : jerky nystagmus ; optic atrophy, 
contracted field of vision. The external recti 
muscles may be paretic or paralyzed. 

8. Myotatic irritability increased, knee- 
jerks exaggerated, ankle-clonus ; contractures 
and muscular rigidity. 

9. Mental impairment in varying degrees. 

10. Vertigo sometimes. 

11. Vesical functions rarely affected. 

12. Apoplectiform seizures do not occur. 



13. Heredity common. 



Disseminated Sclerosis. 

1. (a) Spastic paraplegia; feet close together. 
(6) Ataxic, groggy ; feet wide apart, (c) Ataxic 
paraplegia (a + 6). 

2. Romberg symptom may be present. 

3. Intention tremor ; sometimes ataxy. 

4. Oscillations and jerky movements of the 
head and trunk. 

5. Twitching in facial muscles during 
speaking. 

6. Laborious, scanning, or monotonous 
speech. 

7. Jerky nystagmus; optic atrophy, con- 
tracted field of vision ; ocular nerve palsies. 



8. Myotatic irritability increased 
jerks exaggerated, ankle-clonus ; contractures 
and muscular rigidity. 

9. Mental impairment in varying degrees. 

10. Vertigo common. 

11. Vesical functions more frequently dis- 
turbed. 

12. Apoplectiform seizures occur in a small 
proportion of cases. 

13. Heredity uncommon. 



Disseminated Sclerosis. — The gait in disseminated sclerosis is often 
markedly spastic and paretic — that is, stiff and feeble — and may in 
the early stages of the disease closely resemble that of spastic para- 
plegia due to lateral sclerosis. When the patient attempts to pick 
up a small object with his fingers there are tremor and oscillation 
of the hand. Scanning speech and nystagmus develop later on in 
these cases. It is, however, important to remember that multiple 
cerebrospinal syphilis may closely simulate multiple, or dissemi- 



GAIT 



65 



Haled, sclerosis. Sometimes they may be differentiated by the fact 
that in disseminated sclerosis there is apt to be paresthesia, whereas 

in syphilis there is more apt to be pain. An Important differential 
symptom is thai nystagmus is rare in syphilis, common in dissem- 
inated sclerosis, and ocular palsies are common in syphilis, rarely so 
severe in sclerosis, so that complete oculomotor palsy with ptosis and 
squint would be more likely syphilitic than sclerotic. (See chapter 
on the Eye.) 

Stieglitz has pointed out that in certain cases of acute dissemi- 
nated myelitis and encephalomyelitis following the acute infections 
diseases, the symptoms of an acute or subacute multiple sclerosis 
are presented, more especially the intention tremor, the increased 
reflexes, and the scanning speech. The disease may ultimately 




Fig. 20. — Showing areas of spinal cord involved in ataxic paraplegia, which is practically a 
combination of locomotor ataxia and lateral sclerosis. 1. Lateral or crossed pyramidal tracts. 
2. Posterior columns of Goll and Bnrdach. 3. Direct pyramidal tracts or Torek's columns. 

form the basis of a typical chronic insular sclerosis with its recurrent 
attacks, etc. It may, however — and this is a point of importance — 
subside after a shorter or longer period and end in recovery. 

Myelitis. — In chronic myelitis in the early stages, while motion is 
still preserved, the gait is typically that of feebleness, and the legs 
respond slowly to the cerebral desires, being dragged along after 
the patient, who leans forward, supporting some of his weight on 
crutches or canes. 

Ataxic Paraplegia.— If the lesions of the disease involve the lateral 
pyramidal tracts to a considerable extent, the gait is somewhat 
spastic, and if the sensory fibers are also much involved it may be 
5 



66 



THE FEET AND LEGS 



like that of ataxia. Under these circumstances the attitude and 
gait of a patient are sometimes a combination of those of lateral 
spinal sclerosis (spastic paraplegia) and locomotor ataxia. In some 

instances the spastic symptoms are 
more marked, in others the signs of 
locomotor ataxia are more prominent. 
This condition is called ataxic para- 
plegia, and in it we find the exagger- 
ated knee-jerks of lateral sclerosis asso- 
ciated with the swaying of the body 
(Romberg's symptom) of ataxia. Ankle 
clonus is also present. The crises of 
locomotor ataxia do not occur, and the 
Argyll-Robertson pupil is usually not 
present. (See Fig. 20.) 

Lateral Sclerosis. — In lateral sclerosis 
the gait is typically spastic, the legs 
being rigid from the hip-joint down, and 
the toe being dragged in a semicircle 
from behind forward. 

Polioniyelitis. — When the gait of a 
young child is stumbling, or the leg is 
dragged, or the ankles bend so that 
locomotion is impossible, the probable 
diagnosis is that the cause is acute polio- 
myelitis. (See Paralysis of the Leg.) 

Pseudomuscular Hypertrophy. — In 
pseudomuscular hypertrophy there is 
a peculiar waddling gait, a tendency to 
stumble, the body is usually bent for- 
ward, and there is difficulty in getting 
up from the floor and on going up and 
down stairs. The patient in all his 
movements shows a marked loss of 
power in the legs with a great apparent 
increase in the size of the muscles in 
the legs (Fig. 21). 

The gait of pseudomuscular hyper- 
trophy is sometimes closely reproduced 
in children suffering from severe rickets. 
The other features of the case which 
may mislead the physician are that the 
child, if fat, will have bulging legs, as 
if the muscles were hypertrophied, and lordosis due to spinal weak- 
In the rickety case, however, the knee-jerk is preserved, and 




Fig. 21. — Typical pseudomuscular 
hypertrophy. Note the scoliosis and 
enlarged calves of the legs. (Dercum.) 



ness. 



in the case of pseudomuscular hypertrophy it is lost. 



GAIT 



67 



Infantile Cerebral Paralysis.— The gait of a child suffering from 
infantile cerebral paralysis is quite characteristic. In the first place 
it is spastic, and the patient walks on the toes, or in some cases 
clubfoot develops. The heels are everted and the toes turned 
inward, the knees being so closely approximated that the clothes 
may become worn between them from the rubbing. So great is the 
extension of the legs that the toes arc very apt to drag, and, finally, 
the adduction spasm may be so great that the legs overlap each 
other as walking is attempted (Fig- 22). 




Fig. 22. — Spastic paraplegia; crossed-legged 
progression. (From a patient of Dercum's in 
the Jefferson Medical College Hospital.) 



Fit;. 23. — Side view of a case of paralysis 
agitans, showing forward inclination of trunk. 
Tendency to propulsion. (Dercum.) 



Paralysis Agitans. — In paralysis agitans the patient's gait is 
hurried because, from the bent-over position of his body, his 
centre of gravity is too far forward, and he runs to keep up with it. 
This is called festination. The gait is also somewhat trotting or 
toddling (Fig. 23). 



08 THE FEET AND LEGS 

Cerebellar Disease. — In cerebellar disease the gait may closely 
resemble that of a drunken man, and the patient has the greatest 
difficulty in keeping from sheering off to one side as he walks, 
swaying, too, from side to side (cerebellar titubation). The middle 
lobe of the cerebellum is usually affected; but Nothnagel asserts 
that if these symptoms are associated with paralysis of the oculo- 
motor nerves and other symptoms of brain tumor there is a growth 
in the corpora quadrigemina. 

Hemiplegia. — In hemiplegia the gait is peculiar in the dragging 
along of the paralyzed limb by a peculiar outward swing, which soon 
wears away the sole of the shoe on the inner side near the ball of 
the foot. It is sometimes called a mowing gait, because the leg 
sweeps around in a half -circle. Very often the shoulder opposite the 
paralyzed side is raised in order to tilt the pelvis on the paralyzed 
side, so as to make circumduction easy. 

Hysteria. — The gait of hemiplegia is to be clearly separated from 
that due to hysterical paralysis, for in this condition the leg is 
dragged after the body without this outward swing. It is dragged 
along like the broken hind limb of one of the lower animals, or is 
shoved forward and the well foot drawn after, the reverse of what 
happens in organic paralysis. The footsteps of the hysterical hemi- 
plegic are, moreover, apt to be careful and mincing. Further, the 
loss of power is usually left-sided, and associated with characteristic 
hysterical anesthesia (see chapter on the Skin), and often with areas 
of hyperesthesia. Again, in the gait of hysterical paralysis the 
patient is apt to be excessively laborious in her progress, and will 
exhaust her muscles in her strained movements. An altered 
gait due to irregularly distributed paralysis of groups of muscles 
is nearly always hysterical, and sometimes the patient who has 
hysterical loss of power will suddenly fall through giving way of 
her knees. 

A condition of the gait and station of the patient varying from 
normal, which occurs most commonly in hysteria, consists in an 
inability to coordinate the movements of the muscles of locomotion 
or those used in standing. This is called "astasia abasia." It is 
in reality a form of ataxia often developing only when the patient 
attempts to walk. There is no loss of power in the legs, but an 
inability to use them regularly or with power while walking, although 
if the patient be made to lie down the movements of the limbs as 
made in walking can be performed perfectly. The knee-jerks are 
rarely lost, and in addition the general symptoms of hysteria can 
nearly always be found. The body often reels to and fro, and occa- 
sionally the muscles seem to be somewhat spastic. This symptom 
generally follows some severe shock, and is most commonly seen in 
young persons, usually young women. 



PARM'LKCIA 



69 



Oiteomalacia.— In osteomalacia there is increasing difficulty of 
walking, partly due to pain and partly to muscular weakness. The 
gait is hobbling, tottering, and is made up of short and evidently 
painful steps, "the pelvis and leg being jerked forward as if in one 
piece." The kyphotic deformity of the spine, muscular tenderness, 
and lateral compression of the chest and pelvis, with distortions of 
the limbs, aid in making the diagnosis. 

Rickets. — The gait of rickets is only peculiar when curvature of the 
limbs or spine destroys the normal posture of the body or interferes 
with the movements of the limbs, and it is nearly always more or less 
waddling. 

PARAPLEGIA. „ 



Given a case of paraplegia, or paralysis of the lower extremi- 
ties, What may be its cause? It may arise from a cerebral lesion, 
which is very rare, except in children, when it is common, 1 and 
if cerebral it must depend upon a lesion on both sides of the cere- 
bral cortex or in each capsule; that is to say, there must be present a 
lesion in the leg centres on both sides of the cortex or in the fibers 
going to the legs through the internal capsules. Much more com- 
monly the lesions causing paraplegia are in the spinal cord, very 
rarely this symptom is due to involvement of the nerve trunks on 
both sides, after they have left the cord, and sometimes it is caused 
by hysteria and reflex irritation. 

When paraplegia occurs in a young child it is due in a great 
majority of the cases to caries of the vertebrae, and the pressure so 
produced does not necessarily depend upon compression by the 
bones, but by the inflammatory exudate. 

The spinal lesions giving rise to paraplegia of the lower extremi- 
ties are numerous, and are perhaps best grouped in the following 
table of Bramwell : 

' Inflammation of cord 1 

Softening I Medullary . 
Hemorrhage " " 

Tumors " " J 



1. Organic disease 



2 Functional 



Meningitis " " 
Meningeal hemorrhage 
Injuries 
Tumors 

Caries of bone 
__ Tumors of bone 

f Hysterical. 

J Reflex. 

1 Malarial and anaemic. 

L Dependent on idea. 



Meningeal. 



Osseous. 



i Such an occurrence in adults is very rare, but it is quite common in young children, as 
many as 14 per cent, of the cases of infantile cerebral palsy being paraplegias. (Sachs.) 



70 THE FEET AND LEGS 

Cerebral Spastic Paraplegia.— The paraplegia of cerebral 
infantile paralysis is spastic, and follows difficult labors or injuries 
to the head of the child before or after birth. Contractures nearly 
always ensue, and exist chiefly in the adductors of the thighs, so 
that the attitude is very characteristic (Fig. 24). Epileptic convul- 
sions very often complicate these cases. Often these paraplegias 
are not manifested for some months, or even longer, after' birth. 
In many cases they are first noticed when the child attempts to 
walk. 

Care must be taken not to confuse the contractures which some- 
times develop as the result of the acute anterior poliomyelitis of 
infancy with the spastic state of the muscles arising from infantile 
cerebral paralysis. These contractions with their resulting deformity 
arise in muscles, otherwise healthy, which have been deprived of 
their natural antagonists. These contractures are not spastic and 
often do not occur except upon intention movement. 




Fig. 24. — Spastic diplegia, congenital, presenting choreiform and athetoid movements. 

(Dercum.) 

Arrested Development. — Cerebral spastic paraplegia in infants 
also sometimes comes on in cases of so-called arrested development. 
Such infants present no abnormality for the first few months of life, 
then cease to develop in mental brightness, fail to recognize the nurse 
or mother, cease to play, gradually lose their vision, and develop 
nystagmus. Death usually takes place in one or two years at the 
latest. Convulsions do not occur in this state, but tremors are often 
present in the arms. There is no history in such cases of difficult 
labor or premature delivery. 

Amaurotic Family Idiocy. — Closely allied to this state is that known 
as "amaurotic family idiocy." In this rare condition, only seen so 
far in the children of Hebrew parents, there is in association with 
the symptoms just described a pathognomonic ocular lesion, con- 
sisting in the appearance of a whitish-gray patch in the region of the 
macula lutea, which covers an area nearly twice the size of the optic 



PARAPLEGIA 



71 



disk. In both this and the infantile cerebral form of spastic para- 
plegia the pyramidal tracts are degenerated. 

Care should be taken that the spastic paraplegia of rickets is not 
mistaken for a birth palsy. 

Multiple Sclerosis. — A cerebrospinal cause of spastic paraplegia 
in adults is multiple cerebrospinal sclerosis, in which condition 
the loss of power amounts to a paresis rather than the absolute 
paralysis. The presence of intention tremors, exaggerated knee- 
jerks and ankle clonus, nystagmus, and vertiginous, epileptiform, 
or apoplectiform seizures, with staccato speech, and local areas of 
loss of power elsewhere, associated with the spastic paraplegia, 
renders the diagnosis easy. (See early part of this chapter.) 




Fig. 25. — Shading shows areas involved in lateral sclerosis : 1, the crossed pyramidal tracts; 
2, the direct pyramidal tract of the cervical region, which is affected late in the course of the 



Spinal Spastic Paraplegia. Lateral Sclerosis. — In the adult, 
when there is loss of power in the lower limbs with spastic con- 
traction of the muscles when the patient attempts to move them, 
so that they become rigid, or if before the stage of rigidity develops 
the gait is spastic and stiff and the reflexes are greatly exaggerated, 
the disease is generally lateral spinal sclerosis (Fig. 25). There is 
also in lateral spinal sclerosis absence of both sensory disorders 
and rectal and bladder troubles, but sometimes there are present 
excessively hasty urination and defecation. The reason why the 
reflexes are increased in lateral sclerosis, and similar ailments asso- 
ciated with spastic paraplegia, is that the inhibitory fibers which 
descend from Setschenow's reflex inhibitory centre in the medulla 
oblongata are destroyed in the lateral pyramidal tracts. 



72 



THE FEET AND LEGS 



In amyotrophic lateral sclerosis similar symptoms associated with 
wasting of the muscles are present in the later stages, but in the 
early stages the arms are chiefly affected by the wasting and paralysis 
(Fig. 26). (See chapter on the Hands and Arms.) 

Spinal Pachymeningitis. — Spastic paraplegia may also be due to 
spinal pachymeningitis, and the associated symptoms may so closely 
resemble those of myelitis that a diagnosis is impossible; but the 
spastic character of the paraplegia, the early appearance and severity 
of the pain, and the comparatively slow development of the symp- 
toms in pachymeningitis will aid in separating the two affections, 
as will also the presence of persistently increased reflexes from the first. 
Sensory disturbances, aside from pain, are common in myelitis, but 
rare in this condition. If the inflammatory process becomes wide- 




Fig. 26. — Showing areas of spinal cord involved in amyotrophic lateral sclerosis: 1, anterior 
horns of gray matter containing the trophic cells; 2, crossed pyramidal tracts; 3, the direct 
pyramidal tract. 

spread there may be sensory disorders and trophic sloughs, owing 
to invasion of the portions of the cord connected with the sensation 
and nutrition by a secondary myelitis. The development of signs of 
spinal caries, sepsis, or a psoas abscess in such cases at once shows 
the condition to be meningeal in origin, and the history of trauma- 
tism will point to meningitis rather than myelitis. 

Spinal Syphilis. — Spastic paraplegia, greatly increased tendon 
reflexes, low muscle tension, vesical disorder, and slight sensory 
disturbances in an adult should make the physician think of spinal 
syphilis. 



PARAPLEGIA 



73 



Pott's Disease. — Spastic paraplegia in early childhood, when not 
due to cerebral lesions, as already discussed, is usually due to Pott's 
disease. The reflexes are exaggerated, the hands are drawn up, 
and the feet are extended. If the lumbar cord is diseased, the 
reflexes are lost. Inquiry will perhaps reveal a history that the 
child has been easily tired before the paralysis came on, and has 
complained of bellyache, which has really been due to pain along 
the intercostal nerves from the irritation at their roots. Thus, pain 
in the region of the navel suggests inflammation at the eighth 
dorsal vertebra, or at the ensiform carti- 
lage at the fourth or fifth dorsal vertebra. 
Early in the disease pressure on the 
spinal cord may increase the reflexes. 
The area of the cord involved can be 
determined by the symptoms as detailed 
on pages 81 and 82. The prognosis is 
not always unfavorable, as extraor- 
dinary recoveries take place. 

Hereditary Spastic Paralysis. — Heredi- 
tary spastic spinal paralysis of children 
is to be separated from infantile cerebral 
paralysis by the absence of a history of 
injury to the head at birth, and the 
absence of convulsions and defective 
mental development, all of which ap- 
pear in the cerebral form. This absence 
of convulsions and defective mental 
power in this form of spastic paraplegia 
almost certainly separates it from the 
cerebral infantile type of paralysis. It 
is to be separated from the spastic 
paraplegia of lateral sclerosis by the 
facts that it occurs in early life, and that 
there is a history of heredity, or of sev- 
eral members of the family being affected 
by the disease. There are usually rigidi- 
ties and contractures, but the bladder 
and rectum escape the paralysis, and 
there are no trophic changes. The re- 
flexes are increased. The disease is rare. 

Hysteria. — An important form of contracture following paralysis 
or occurring without it, prone to lead to a mistake in diagnosis, is 
that seen in hysteria (Fig. 27). As a rule, the contractures come 
on in association with paraplegia. Sometimes, however, they affect 
the arms or an arm. It is a characteristic of these contractures 




Fig. 27. — Hysterical spasm and 
contracture, showing attitude in 
erect position. (Bramwell.) 



74 THE FEET AND LEGS 

due to hysteria that they set in suddenly, and are always accompanied 
by such hysterical symptoms as borborygmi, ovarian tenderness, 
and often areas of anesthesia. Weir Mitchell has divided these 
cases into two forms. The first only involves single parts or limited 
muscle groups, and, though the contractures may last for years, 
joint or muscle changes do not occur. In the second class, one limb 
after another is attacked until all means of locomotion, or even 
moving the trunk, are lost, and the muscles, joints, and areolar tissue 
undergo organic changes. The reflexes are lost in such cases in 
the late stages, and the electrical reaction of the muscles is impaired. 
The diagnosis is to be reached by the sex, the personal history, the 
history of the illness, the presence of anesthesia (see chapter on Skin), 
and hyperesthesias. Usually the contracture comes on suddenly; 
it is very rigid, and the muscles on both sides of the limb are fixed — 
that is, the contracture involves antagonistic muscles. Sleep does 
not always cause a relaxation of hysterical contraction, but ether or 
chloroform usually does so. (See chapter on the Hands and Arms.) 

Transverse Myelitis. — In transverse myelitis there is often in the 
later stages of the malady spastic paraplegia as a result of the irrita- 
bility of the spinal centres below the seat of the lesion, which may 
cause a spastic state of the muscles. In distinction from lateral 
sclerosis we find in myelitis that there are girdle pains, involvement 
of the bladder and rectum, and sensory paralysis. 

Spastic Monoplegia or Single Contracture.— Spastic monoplegia 
may arise from several causes. It may develop as a manifestation 
of progressive muscular atrophy in those rare cases in which the 
disease begins first in a lower limb, the so-called peroneal, or leg, form 
of the disease. The extensor muscles of the toes lose their power, 
the interossei waste, the foot may be flattened or claw shaped, or, 
in other instances, any one of the forms of clubfoot may develop. If 
the deformity is bilateral, it is a strong evidence of its being the leg 
type of progressive muscular atrophy, and that it is not due to acute 
infantile paralysis. There will probably be a history of heredity 
in such cases. This state of the foot must be carefully separated 
from the pes equinus seen as a result of acute infantile spinal 
paralysis involving the tibialis anticus. The toes are hyperextended, 
and the foot is very broad when viewed from side to side at the meta- 
tarsal joints. It is stated that this sign is considered characteristic 
of the early development of the disease in families with the heredity. 
Sometimes in place of this deformity the foot becomes almost parallel 
with the tibia in excessive extension, with eversion as the result of 
shortening of the peroneus longus. In other instances the deformities 
undergo marked changes as the disease progresses, so that they 
not only grow worse, but are altered in type. In distinction from 
ordinary progressive muscular atrophy this leg type often has marked 
disturbance of sensation associated with it. (Dana.) It generally 



PARAPLEGIA 7." 

occurs in males. According to Marie, another form of clawfoot 
is seen in Friedreich's ataxia, there being associated with it clubfoot. 

Progressive muscular atrophy of the peroneal type is a rare 
disease, which must be separated from multiple neuritis by 
the pain of the latter affection and the fact that neuritis rarely 
produces double clubfoot, and, further, that in neuritis there is 
no history of heredity. From poliomyelitis we separate it by the 
fact that in this peroneal type of paralysis the onset is more slow and 
by the fact that there is a loss of the reflexes in severe poliomyelitis, 
though they are preserved for a long time in the peroneal type. 
From Friedreich's ataxia it is separated by the fact that in that 
disease the reflexes are lost, there is a peculiar unsteadiness in walk- 
ing, and an absence of electrical changes in the muscles. 

A shrivelled, undeveloped foot and leg with drawing up and 
deformity are seen most commonly as the ultimate result of the 
acute cerebral paralysis of infancy. 

Deformity or distortion of the legs may result from the secondary 
muscular atrophy following upon chronic inflammation in a joint 
or joints. The muscular wasting under these circumstances may 
arise from neuritis, which is associated with tin' arthritis, but its 
cause is often difficult to discover. 

Non-spastic Paraplegia. — Passing from spastic paraplegia we 
come to those forms of paraplegia lacking this peculiarity. They 
are quite numerous and important. If the paraplegia comes on 
suddenly the cause may be hemorrhage into the substance of the 
cord or into the spinal membranes, or be due to compression or 
destruction of the cord by injuries of the back, whereby there is 
laceration of the soft parts or fracture or dislocation of the vertebra 4 , 
or it may be due to acute transverse myelitis. 

When the paraplegia is slower in onset but not sudden, the spinal 
causes are acute ascending paralysis or Landry's paralysis, acute 
central myelitis, and acute transverse myelitis. On the other hand, 
the slowly oncoming non-spastic paraplegias are dtte to chronic mye- 
litis, to locomotor ataxia, poliomyelitis, neuritis, and pressure due to 
disease of the vertebra? or to spinal tumors. Finally, we have what 
are called reflex and hysterical paraplegias. 

Hemorrhage into the Spinal Cord. — Hemorrhage into spinal cord 
is an exceedingly rare condition unless preceded by grave disease 
of its tissues. Indeed, the existence of such a condition in man has 
been denied. The patient, previously in good health, is stricken 
suddenly to the ground, and there may be almost as much cerebral 
disturbance as in cerebral apoplexy, but consciousness is generally 
preserved. The amount of paraplegia may be instantly complete, 
or not be complete for twenty-four hours. Bed-sores speedily 
develop, and death ensues from exhaustion or from extension of 



76 THE FEET AND LEGS 

the hemorrhage upward to the vital centres. Practically identical 
symptoms ensue when the hemorrhage takes place between the 
membranes covering the cord. In both instances the reflexes are 
lost if the hemorrhage be sufficient to produce total paralysis. 

Acute Ascending Myelitis.— If , on the other hand, after a prodromal 
period of short duration, during which there is some fever, the patient 
is suddenly attacked with paraplegia, the cause may be the acute 
ascending myelitis of Landry, and the rapid extension to the trunk, 
the arms, and the respiratory muscles, with the consequent early 
death of the patient, will confirm the diagnosis. There is usually no 
involvement of sensation or trophic paralysis, and the sphincters of 
the bladder and rectum escape the paralysis. Landry's paralysis 
is very rare. Similar symptoms associated with sensory disturbances 
are probably due to a polyneuritis. 

Diller and Meyer state that the cardinal points for diagnosis of 
Landry's paralysis are: 

1. Flaccid paralysis of the muscles, spreading rapidly from one 
point over the rest of the body, generally beginning in the legs, but 
sometimes following the reverse order, as in the French zoologist 
Cuvier. 

2. Absence of muscular atrophy and of electrical reaction of 
degeneration. 

3. Tendon and superficial reflexes absent. 

4. Sensibility not, or only slightly, impaired. 

5. Sphincters, as a rule, intact (exceptions rather frequent). 
Myelitis. — By far the most common cause of paraplegia is myelitis 

in one of its forms ; but whether the onset be rapid or slow, it must 
be remembered that the symptoms of myelitis depend, first, upon the 
level at which the spinal cord is involved, and, second, upon whether 
the lesion involves the white matter or the gray. If the lesion is 
an acute central myelitis of the gray matter, it usually produces 
many of the symptoms about to be detailed under acute transverse 
myelitis, but the onset is malignant and the areas involved are 
usually widespread. It is attended by fever of a marked type, 
though the temperature of the paralyzed parts is below normal, and 
by early evidences of trophic lesions. Multiple arthritis may come 
on. The bladder and rectum are paralyzed, and, finally, delirium 
may develop. The prognosis is unfavorable. Acute central mye- 
litis is to be separated from Landry's paralysis by the facts that in 
it sensation is lost, and there are rectal and vesical paralysis, fever, 
and rapid trophic changes. From polyneuritis it is separated by the 
facts that there are no great trophic changes in this form of neuritis, 
and the rectum and bladder are rarely paralyzed. 

The symptoms of acute transverse myelitis are capable of being 
divided into three groups, in the first of which the onset is as sudden 



PARAPLEGIA 77 

as is that of apoplexy, in the second the symptoms come on quickly, 
and in the third, more subacutely. In the acute forms, however, 
the history will be that after a period of numbness, heaviness, and 
weakness of the legs, with more or less pain in the back, the patient 
has found it impossible to move his legs, has lost control of his blad- 
der and rectum, or suffers from retention of the urine and feces 
instead, and at the same time has developed anesthesia of his lower 
extremities and the girdle sensation, or, if the lesion be situated 
high up in the cord, tingling in his arms. (See chapter on the Skin.) 
The reflexes may be abolished at first, and then return in an exag- 
gerated form in the segments of the cord below the area affected. 
In other cases the reflexes do not return if the lesion is completely 
transverse. The patient is speedily bedridden, and to these symp- 
toms just detailed is soon added the development of bed-sores and 
sloughs on dependent parts of the legs or on the buttocks, followed, 
it may be, by death from exhaustion, although the case may survive 
for months and even become somewhat better. If improvement 
takes place, sensation returns in the course of from one to six months, 
some motion in from six to eighteen months, and, finally, spasms 
and contractures may result from descending degeneration of the 
lateral tracts. 

In cases in which paraplegia results from the more subacute form 
of transverse myelitis the symptoms are usually not quite so rapid 
in their onset as in the type just named. The patient first notice's 
that his bladder and rectum are unduly irritable, and in his limbs 
there may be subjective sensory disturbances. (See Paresthesia, in 
chapter on the Skin.) The motor symptoms begin by a feeling of 
heaviness or inability to quickly move the lower limbs, so that the 
patient feels tired on slight exertion. Soon these symptoms deepen 
into absolute anesthesia and motor paralysis, and the girdle sensation 
on the trunk becomes well developed. (See chapter on the Skin.) 
The bladder, which at first was irritable, may now be toneless, 
paralyzed, and retentive or incontinent: retentive if the lesion is 
above the lumbar cord, and incontinent when the lower part of the 
lumbar enlargement is diseased. The reflexes at first may be abol- 
ished, but very soon some of them return, only those reflexes the 
centres for which are destroyed by the transverse lesion being abol- 
ished; that is, the reflexes recover after the first shock of the attack, 
and those muscles and tendons having spinal centres below the lesion 
have their reflexes increased because they are cut off from the inhib- 
iting centres higher up in the cord or medulla. The muscles of the 
legs, which at the first shock of the onset of the malady were all 
flaccid and paralyzed, now divide themselves into two classes: those 
that are connected with the diseased part of the cord, w T hich remain 
paralyzed, and those which are connected with the lower centres, 



78 



THE FEET AND LEGS 



which recover some power; but as the lesion is so placed as to cut off 
all off them from cerebral influences, voluntary motion is lost as 
completely as if all were deprived of spinal influence. The truly 
paralyzed muscles waste, but the others which have unimpaired 
spinal centres do not, except very slowly from disuse. On the 
contrary, they often become spastically contracted. Other trophic 
changes, such as bed-sores and bullae, develop in the skin connected 
with the diseased focus, but not in the skin connected with centres 
below the lesion. Anesthesia is present because the lesion prevents the 
sensory impulse from reaching the brain. (See chapter on the Skin.) 
The following diagram from Seymour Taylor's Index of Medicine 
presents the symptoms of a lesion in the spinal cord in transverse 
myelitis. 

Symptoms in Transverse Myelitis. 

The darkened portion represents the seat of lesion. 

Spinal cord. 



Reflexes normal 






Reflexes normal. 


Band of hyperesthesia .... 






Band of hyperesthesia. 


f Muscles palsied, waste, and lose 

8 1 

a 1 their electrical reactions . . 

'E- 






Muscles palsied, waste and lose 


■ 


■ 


their electrical reactions. 


t 1 

« | Reflexes lost ......... 


■ 


1 


Reflexes lost. 


H 1 

L Sensation lost ....... 


■ 


■ 


Sensation lost. 


Muscles palsied 






Muscles palsied. 


Do not waste ....... 






Do not waste. 


No loss of electrical reactions . 






No loss of electrical reactions. 


Reflexes increased 






Reflexes increased. 


Sensation lost 






Sensation lost. 


Bedsores 






Bedsores. 


Temperature above rest of body 


Temperature above rest of body 



When the entire cord is not evenly involved in the transverse 
lesion certain groups of muscles partly escape. It is asserted that the 
extensors escape oftener than the flexors. The height of the par- 
alysis also depends upon the situation of the lesion of the cord, and if 
high enough to involve the cervical region, and yet not high enough 
to paralyze the diaphragm and cause death (third or fourth cervical), 
there may be contraction of the pupil by involvement of the fibers 



PARAPLEGIA 



79 



from the nucleus of the third nerve, 
which runs down the cord to the 
last cervical vertebrae before join- 
ing the sympathetic. When the 
legs become spastic late in trans- 
verse myelitis the cause is supposed 
to be a descending degeneration in 
the pyramidal tracts. 

The symptoms of chronic trans- 
verse myelitis producing paraplegia 
are practically identical with the 
more acute form just described, 
except that they are very slow in 
their development. 

The Seat of the Lesion. — Having 
discussed the various forms of 
myelitis, we have still to study the 
question of the seat of the lesion. 
Before doing this, it is to be re- 
membered, in studying the relation- 
ship of the spinal cord to the verte- 
brae, that the so-called segments of 
the cord in no way correspond with 
the various segments of the spinal 
column bearing similar names. Thus 
the cord extends only to the level of 
the upper part of the second lumbar 
vertebra, although the spinal canal 
reaches much lower than this. There 
are thirty-one segments of the cord, 
each of which gives off a pair of 
spinal nerves. The first segment 
of the cord is at the foramen 
magnum and the last at the second 
lumbar vertebra. 

This is well shown in the accom- 
panying figure, modified from one 
by Gowers (Fig. 28). 

Not only is this true, but the 
nerves do not emerge from the spinal 
canal where they leave the cord, 
but at a lower level. In the case 
of the lumbar and sacral segments 
of the cord the nerves form a bundle 
which extends down the remaining 
part of the spinal canal. 




-Showingj-elation of.segments of 
cord to vertebra? and relation of spinal 
nerve roots to the cord and their levels ot 
exit (modified from Gowers). The fisiurcs 
to the left refer to the spines of the vertebra?, 
the next column of figures to the segments 
of the cord, the next columu to the bodies 
of the vertebra?, and the last fignres to the 
right to the spinal nerves. 



80 



THE FEET AND LEGS 



There are two areas in the cord of greater importance than the 
others, namely, the cervical enlargement, which gives off the nerves 
to the upper extremities, and the lumbar enlargement, which sup- 
plies the lower extremities. The eighth cervical and first dorsal 
segments of the cord lie opposite the spine of the seventh cervical 
vertebra and the lumbar-sacral enlargement opposite that of the 
spine of the tenth dorsal vertebra. 

Let us suppose that a patient presents himself with the following 
condition : There is complete paralysis of his arms and legs, with 
paralysis of the muscles of the trunk, and total anesthesia of the 
same areas. The legs are in a state of spastic paralysis, their reflexes 



8th cervical and 1st dor 
sal segment at 7th ver 
tebra. 



Lumbar enlargement of 
cord at 10th dorsal ver- 
tebra. 



End of cord at 2d lumbar ) 
vertebra. / 



Cauda equina 




1st to 7th cervical 
vertebra. 



1st to 12th dorsal 
vertebra. 



1st to 5th lumbar 
vertebra. 



1st to 5th sacral 
vertebra. 



Fig. 27.— Showing the surface areas of the back corresponding approximately to the areas of 
the spinal cord supplying the trunk and limbs, according to the diagram on the preceding page. 

are increased, and their nutrition is unimpaired; although the arms 
are found relaxed and flaccid, devoid of reflex excitability, and under- 
going degenerative atrophy. The bladder and rectum are not 
retentive. All these symptoms point to a transverse lesion of the 
spinal cord in the cervical region, probably between the fifth cervical 
and first dorsal vertebrae. 

If, on the other hand, the upper extremities are not affected 
(except, perhaps, the small muscles of the hand), but there is the 
same loss of power in the legs, with spastic contraction of the 



PARAPLEGIA 



81 



muscles, and the other symptoms just named are present, combined 
with degeneration of the muscles of the trunk, the lesion is probably 
somewhere between the second and twelfth dorsal vertebrae. 

Again, if the paralysis of motion and sensation be only in the 
lower limbs, and there be flaccidity of the muscles (where before 
we discovered spastic contraction), with muscular degeneration, loss 
of reflexes, and paralysis of the bladder and rectum, the lesion is 
between the tenth dorsal and first lumbar vertebra. 

Still further, if there be loss of power with degeneration of the 
small muscles of the feet, and loss of sensation of the outside of the 
feet and toes, and of the skin about the anus, with preservation of 
power in the thighs and of the patellar reflex, the lesion is at the 
end of the cord in the area of the cone. 

In this connection the reader should study that part of the chapter 
on the Skin which deals with anesthesia. 

Differential Diagnosis of Lumbar, Dorsal, and Cervical 

Myelitis. 1 



Paralysis. 



Sensation. 



Atrophy. 



Lumbar myelitis. 



Paraplegia. 



Pains in legs, or girdle-pains 
around loins ; hyperaesthe- 
tic zone around loins ; an- 
aesthesia of legs, complete 
or uneven distribution. 



Of legs. 



Dorsal myelitis. 



1. Dorsal, abdominal, and 
intercostal muscles, ac- 
cording to height of lesion. 

2. Legs. 

Girdle-pain and hyperaes- 
thetic zone between ensi- 
form cartilage and pubes. 



Cervical myelitis. 



Neck-muscles, dia- 
phragm, arms, trunk, 
and legs. 



Hyperesthesia and 
pains in certain 
nerve-distributions 
of arms ; below this 
anaesthesia of arms, 
body, and legs. 

Of dorsal and abdominal Atrophy of neck-mus- 
(and intercostal muscles cles ( rare ) or more 
not subject to examination) commonly of arms, 
corresponding to height of 
lesion ; sometimes mild 
and slow of legs. 



Electrical 
reaction. 


R. D. in atrophied muscles ; 
or in mild cases quantita- 
tive diminution. 


Bladder. 


Incontinence from paralysis 
of sphincter. 


Bowels. 


Incontinence from paralysis 
of sphincter; disguised by 
constipation. 


Reflexes, 
superficial, 


Lost. 


Reflexes, 
deep. 


Lost. 


Priapism. 


Absent. 



R. D. in dorsal and abdomi- 
nal muscles; slight quanti- 
tative changes only in legs 
when wasted. 



R. D. in atrophied 
muscles. 



Retention, or intermittent Same as in dorsal mye- 
incontinence from reflex f litis, 
action ; later from over- 
flow. Cystitis common. 



Same as in dorsal mye- 
litis. 



Involuntary evacuation 
from reflex spasm or con- 
stipation. 

Temporary loss, then rapid j Same as in dorsal mye- 
increase. litis. 

Temporary loss, then slow i Same as in dorsal mye- 
increase. I litis. 



Often present. 



Often present. 



From Prince's article in Dercum's Nervous Diseases, 



82 



THE FEET AND LEGS 



Localization of the Functions of the Segments of the Spinal 
Cord. (According to Starr ) 



Segment. 



II. and III. 

Cervical. 



IV. 

Cervical. 



V. 
Cervical. 



Muscles. 



VI. 

Cervical. 



VII. 

Cervical. 



VIII. 
Cervical. 



I. Dorsal. 



II. to XII. 
Dorsal. 



I. Lumbar 



II. 
Lumbar. 



Sterno-mastoid. 
Trapezius. 
Scaleni and neck. 
Diaphragm. 

Diaphragm. 

Deltoid. 

Biceps. 

Coraco-brachialis. 

Supinator longus. 

Rhomboid. 

Supra- and infra spinatus. 

Deltoid. 

Biceps. 

Coraco-brachialis. 

Bracnialis amicus. 

Supinator longus. 

Supinator brevis. 

Rhomboid. 

Teres minor. 

Pectoralis (clavicular part). 

Serratus magnus. 

Biceps. 

Brachial is anticus. 

Pectoralis (clavicular part). 

Serratus magnus. 

Triceps. 

Extensors of wrist and 

fingers. 
Pronators. 

Triceps (long head). 
Extensors of wrist and 

fingers. 
Pronators of wrist. 
Flexors of wrist. 
Subscapular. 
Pectoralis (costal part). 
Latissimus dorsi. 
Teres major. 

Flexors of wrist and fingers 
Intrinsic muscles of hand. 

Extensors of thumb. 
Intrinsic hand muscles. 
Thenar and hypothenar 
eminences. 

Muscles of back and abdo- 
men. 
Erectores spinse. 



Ilio- psoas. 
Sartorius. 
Muscles of abdomen. 



Ilio-psoas (sartorius). 
Flexors of knee (Kemak; 
Quadriceps feuioris. 



Hypochondrium. (?) 

Sudden inspiration produced 
by sudden pressure beneath 
the lower border of ribs. 

Pupil. 4th to 7th cervical. 

Dilatation of the pupil pro- 
duced by irritation of the 
neck. 



Scapular. 

5th cervical to 1st dorsal. 

Irritation of skin over the 
scapula produces contrac- 
tion of the scapular mus- 
cles. 

Supinator lonsus. 

Tapping its tendon in wrist 
produces flexion of fore 
arm. 

Triceps. 

5th to 6th cervical. 

Tapping elbow tendon pro- 
duces extension of forearm 

Posterior wrist. 

6th to 8th cervical . 

Tapping tendons causes ex- 
tension of hand. 

Anterior wrist. 
7th to 8th cervical. 
Tapping anterior tendons 

causes flexion of wrist. 
Palmar. 7th cervical to 1st 

dorsal. 
Stroking palm causes closure 

of fingers. 



Epigastric. 4th to 7th dorsal. 
Tickling mammary region 

causes retraction of the 

epigastrium. 
Abdominal. 7th to 11th dor- 
sal. 
Stroking side of abdomen 

causes retraction of belly. 

Cremasteric. 2d to 3d lum- 
bar. 
Stroking inner thigh causes 
retraction of scrotum. 

Patellar tendon. 
Striking tendon causes ex- 
tension of leg. 



Sensation. 



Back of head to vertex. 
Neck. 



Neck 

Upper shoulder. 

Outer arm. 



Back of shoulder and 

arm. 
Outer side of arm and 

forearm, front aud 

back. 



Outer side of forearm, 

front and back. 
Outer half of hand. 



Inner side and back of 
arm and forearm. 

Radial half of the 
hand. 



Forearm and hand, 
inner half. 

Forearm, inner half. 
Ulnar distribution to 
hand. 



Skin of chest and 
abdomen, in bands 
running around and 
downward corre- 
sponding to spinal 
nerves. 

Upper gluteal region. 



Skin over groin and 
front of scrotum. 



Outer side of thigh. 



PARAPLEGIA 



83 



This subject is still further subdivided and elucidated by the 
above table and by Fig. 27. 

Finally, it is possible for disease of the cauda equina to produce 
symptoms of a lumbar-sacral lesion, owing to the fact that this 
hi 1 1 idle is composed of fibers derived from these two areas. The 
patellar reflex may be preserved, as the lesion is below the reflex 
arc, and all the fibers may not be involved. 



Segment. 


Muscles. 


Reflex. 


Sensation. 


III. 

Lumbar. 


Quadriceps femoris. 
Inner rotators of thigh. 
Abductors of thigh. 




Front and inner side 
of thigh. 


IV. 
Lumbar. 


Abductors of thigh. 
Adductors of thigh. 
Flexors of knee (Ferrier). 
Tibialis anticus. 


Gluteal. 

1th to 5th lumbar. 
Stroking but lock causes 
dimpling in fold of buttock. 


Inner side of thigh and 
leg to ankle. 
Inner side of foot. 


V. 

Lumbar. 


Outward rotators of thigh. 
Flexors of knee (Ferrier). 
Flexors of ankle. 
Extensors of toes. 




Back of thigh, back of 
leg. and outer part of 
foot. 


I. to II. 
Sacral. 


Flexors of ankle. 

Long flexor of toes 

I'eronei. 

Intrinsic muscles of foot. 


Plantar. 

Tickling sole of foot cm uses 
flexion of toes and retrac- 
tion of leg. 


Back of thigh. 

Leg and toot, outer 

side. 


III. to V. 
Sacral. 


Perineal muscles. 


Foot reflex. Achilles tendon 
Overextension of fool causes 
rapid flexion; ankle clonus 
Bladder and rectal centres. 


Skin over sacrum. 
Anus. 

Perineum. Genitals. 



Locomotor Ataxia. — Paraplegia when due to locomotor ataxia is 
nearly always so surrounded by other typical symptoms of this 
disease as to render easy its separation from the paraplegia of myelitis, 
and, further, there is rarely a true loss of power. The stabbing 
and darting pains of ataxia (see chapter on Pain), the presence of 
the Argyll-Robertson pupil, the absence of the patellar reflex, and 
the atrophy of the optic nerve are all characteristic of ataxia, and 
are absent in myelitis. (See early part of this chapter on Gait.) 

Ataxic Paraplegia. — The symptoms of lateral sclerosis and amyo- 
trophic lateral sclerosis have already been discussed under Gait 
and Spastic Paraplegia, but in the paraplegia called ataxic para- 
plegia, also already discussed, there are in association lateral sclero- 
sis and posterior sclerosis, and for this reason some of the symptoms 
of both are found to be present. Thus, in addition to loss of power 
there is a spastic condition of the legs with exaggerated reflexes, 
absence of the Argyll-Robertson pupil and of crises of pain, but 
the Romberg symptom, or swaying when the eyes are closed, is 
present. The condition which most closely resembles ataxic para- 
plegia is that of tumor of the middle lobe of the cerebellum, but in 
such cases we have, in addition, headache, vertigo, optic neuritis, 
titubation, and sometimes vomiting. 



84 THE FEET AND LEGS 

Poliomyelitis.— The onset of paraplegia in a young child, pre- 
ceded by an attack of fever, vomiting, restlessness, and general illness, 
lasting but a few hours or days, and which may be complicated by 
convulsions, all point to the cause being poliomyelitis of a severe type. 
The legs are, however, as a rule, only completely paralyzed for a 
brief period after the attack. Eventually the storm clears off, and 
only the muscles directly connected with the diseased cells in the 
cord (anterior cornua) remain paralyzed. There is no loss of sen- 
sation, but reflex action is abolished in the paralyzed parts. Far 
and away the most important point in the diagnosis is the symptom 
of rapid wasting of the muscles in the paralyzed parts and the rapid 
development of coldness in these areas, which is due to the destruc- 
tion of the trophic centres in the spinal cord. (See Fig. 30.) 

Paraplegia Resulting from Tumor of the Cord or its membranes 
only ensues when the growth is so placed as to cut off all the motor 
tracts supplying both limbs, which is rarely accomplished until after 
a long history of more or less well-developed motor and sensory 
failure. The paralysis is developed in the areas supplied by the 
centres in the cord below or at the level of the growth, and the 
violent pain nearly always present in cases of tumor points to the 
diagnosis. Very painful paraplegia, therefore, indicates spinal 
tumor as its cause. The areas of anesthesia and the muscles involved 
may also give definite information as to the seat of the growth. (See 
chapter on the Skin, and Starr's table just quoted.) 

Fracture of Vertebrae. — If the paraplegia be due to compression 
from fracture or dislocation of the vertebras or to other direct 
injury the history of the patient and the evidences of external local 
mischief will decide the diagnosis. 

Reflex Paralysis. — Very rarely during the course of severe disease, 
producing irritation of the bladder, kidney, bowels, or rectum, as in 
violent cystitis, stone in the kidney, and dysentery, paraplegia comes 
on, due in some cases to an infectious myelitis, but in others to 
what is apparently only a reflex paralysis, as it often passes away with 
the removal of the source of irritation. Even worms in the intestine 
are said to have produced such a paralysis, and their removal has 
been followed by cure. Generally sensation in the limbs is unim- 
paired and the bladder and rectum act normally. Sometimes, how- 
ever, in the presence of severe renal disease, as renal calculus, there 
may be all sorts of disturbance of sensation and pain, as well as great 
motor paralysis, with total loss of reflexes, following an exaggeration 
of the reflexes. Probably these severe cases are always due to a 
coincident myelitis rather than to a reflex irritative cause. 

Hysteria. — No form of paraplegia presents so many types or repre- 
sents so many organic diseases as does that due to hysteria, for there 
may be not only great loss of motion, but exaggerated or lost reflexes 



PARAPLEGIA Ho 

relaxation or spastic contraction of the muscles, anesthesia and hyper- 
esthesia, pain or no pain. The very occurrence of such irregular 
manifestations in a young, neurotic girl, the fact that the anesthetic 
areas constantly tend to shift their position, and, finally, that the 
contractures, if present from hysteria, disappear on administering an 
anesthetic to a stage in which muscular relaxation is produced in the 
ordinary individual, aid us in making a diagnosis. (See that part 
of this chapter on Contractures.) 

Scurvy. — A pseudoparalysis of the legs with immobility sometimes 
occurs as a symptom of scorbutus in infancy. The parents notice that 
the child flinches when it is picked up or handled, and seems as if 
tender from rheumatism. Often the gums are swollen and bleeding, 
and purpuric eruptions appear on the skin. The shafts of the bones 
of the legs or of the arms may be enlarged, and hematuria or bloody 
stools may appear. 

Rickets. — Pseudoparaplegia may also occur in rickety children 
from faulty muscular and bony development. It is to be separated 
from the ordinary paraplegias of childhood by the state of the bones, 
the presence of knee-jerks, and the absence of local wasting or spasm 
although general spasms, or capropedal spasm, is often seen in 
rickety children. 

Diphtheritic Paralysis. — Not uncommonly a partial paraplegia 
occurs as a result or sequel of diphtheria. The condition, however, 
is more ataxic than paraplegic, and Bourges asserts that there is no 
muscular atrophy such as occurs in true paraplegia due to neuritis, 
or in that due to some spinal lesions. 

Neuritis. — When neuritis produces sudden paraplegia the symp- 
toms very closely resemble those of acute myelitis. Neuritis may 
also cause pseudotabes if its onset is slow. The neuritis is always 
multiple and involves the arms and the body after affecting the legs; 
there is w r ell-developed anesthesia (see chapter on the Skin), preceded 
by sensory disturbances and marked muscular and nerve-trunk ten- 
derness; but there is no girdle sensation, as there is in myelitis 
and tabes. There are often trophic changes in the skin in neuritis 
(see chapter on the Skin), but no bed-sores as in myelitis. J. M. 
Da Costa stated that malarial neuritis may cause paraplegia of the 
lower limbs, but, as a rule, toxic neuritis produces loss of power in the 
arms. Very rarely paraplegia of the lower extremities results from 
diabetes mellitus, the lesion being in all probability a multiple neuritis. 

Family Periodic Paralysis. — A very rare condition, involving not 
only the legs, but the entire body, is what is called family periodic 
paralysis, in which flaccid motor paralysis, with loss of electrical 
reaction and reflex activity, comes on suddenly, lasts for a few 
hours or days, and is then followed by perfect health. It is always 
hereditary. 



86 



THE FEET AND LEGS 



Monoplegia of a Lower Extremity may be due to a cerebral 
lesion or to spinal or nerve-trunk lesions. The cerebral lesion 
producing monoplegia in one leg is very rare, and if it occurs, at 
any age, indicates a lesion in the convolutions at the upper end of 
the fissure of Rolando, and the continuation of this area in the 
paracental lobule of the marginal convolution. Unlike the para- 
plegias of infantile cerebral paralysis, monoplegia of the leg very 
rarely arises from this cause. If there are no signs of cerebral 
trouble, the presence of a complete leg monoplegia can mean one of 
several things, namely, a lesion limited to one side of the cord, as, 
for example, a hemilateral myelitis, hysterical paralysis, in which 
there will be irregular anesthesia (see Chapter on the Skin), and the 
other hysterical signs, or a tumor pressing on the crural nerve in the 
pelvis, or section of the nerve by injury. Apparent monoplegia 
may, however, be due to muscular pain or a painful phlebitis 
producing muscular fixation. 

Diagram showing Symptoms in Hemilateral Myelitis. 1 

(The darkened mass represents the site of the lesion.) 

Spinal cord. 



Reflexes normal 

Band of hyperesthesia .... 

Band of anaesthesia 

Reflexes lost 

Motor palsy 

Hyperesthesia 

Reflexes increased 

Temperature above that of the 
rest of the body 



I 



Reflexes normal. 
Band of hyperesthesia. 
Band of anesthesia. 

Motor power unaffected. 

Anesthesia. 

Reflexes unaffected. 

Temperature same as that of 
the rest of the body. 



If the condition is due to a lesion on one side of the cord, the 
symptoms are quite characteristic. There is paralysis of all the 
muscles of the leg which are supplied by the part of the cord affected 
or below it. The muscles, the nerve supply of which comes directly 
from the affected part, eventually waste and undergo degenerative 
changes. The most typical symptom of this lesion is, however, 
the crossed character of the sensory paralysis. That is to say, there 
is loss of sensation in the limb opposite that in which motion is lost, 
and in the limb in which motion is lost there is hyperesthesia, so that 
the lightest touch may be very painful. The cause of this is obscure, 



From Seymour Taylor's Index of Medicine. 



Paraplegia 



87 



for the studies of Mott have proved that the sensory tracts in the cord 
do not decussate on entering it, as has been supposed heretofore. 
There is, however, a symmetrical band of anesthesia round the body 
at the level of the lesions, and a similar band of hyperesthesia above 
the lesions. The reflexes of the parts supplied by the diseased area 
are lost, but those supplied by the area below the lesions are increased 
as in ordinary myelitis. Very commonly the paralyzed limb is 
over-warm from vasomotor palsy. 

Paralysis of Certain Groups of Muscles or a single muscle in the 
legs is most commonly due to anterior poliomyelitis or neuritis (Fig. 
30). In poliomyelitis the child will be found to have loss of power 
in certain muscles in one or both legs (see also Paraplegia), so that 




Fig. 30.— Areas involved in acute and chronic poliomyelitis. In children it is sometimes 
called acute infantile paralysis. The shaded areaiudicates the cells in anterior cornua of gray 
matter which are involved. 

there is a dragging of the toe, or " foot-drop," the shoe becomes 
irregularly worn through, being dragged on one edge along the 
ground, the involved muscles being peculiarly relaxed and flaccid, 
so that the leg may waddle, to use a crude term. This is sometimes 
called a "Punchinello leg." There is no tendency to spastic con- 
traction, the reflexes are rapidly lost in the affected part, and the 
muscles speedily waste and develop the reaction of degeneration 
When contractures take place they are not spastic, but are due 
to healthy muscles being unopposed by the diseased ones. The 
temperature of the paralyzed part is lower than normal. The history 
in poliomyelitis is that of sudden onset, with fever, vomiting, and 
restlessness. The two conditions of acute cerebral paralysis and 



88 THE FEET AND LEGS 

anterior poliomyelitis are so clearly separated in well-marked cases 
that no error can be made, particularly if the history of the attack 
be borne in mind, unless it be in the obscure forms of cerebral in- 
fantile palsy in the early stages. In acute infantile paralysis of spinal 
origin the right lower extremity is most frequently affected, after this, 
a close second, the left leg. Sometimes muscular atrophy may be 
masked in young children- by the abundance of subcutaneous fat. 
A point of some importance in examining the reflexes is that pres- 
ence of knee-jerk should not exclude the diagnosis of poliomyelitis, 
because the reflex act is only destroyed if the centres which are con- 
cerned in this jerk are diseased — that is, if the disease has only affected 
that part of the cord supplying the foot, a tap on the knee may readily 
produce a response, whereas if the disease be higher up in the cord 
the reflex will be lost. The chronic anterior poliomyelitis of adult 
life presents very similar symptoms to the acute form of infancy, 
but is a very rare disease. 

Care must be taken that paralysis of the leg resulting from an 
injury to the peroneal nerve with resulting neuritis is not mistaken 
for acute poliomyelitis. The history of an accident, of pain, swell- 
ing, and the presence of a bruise aid us in making a diagnosis. 
If these symptoms occur in an adult, a possible cause is paralysis 
of the peroneal nerve occurring in the course of tabes. (In connec- 
tion with this chapter see that on the Significance of Anesthesia of 
the Skin.) 

Deformities of the Feet and Legs.— Much of what has been 
said in the preceding chapter as to the diseases which produce altera- 
tions in the shape of the hand and arm applies equally to the changes 
from the normal seen in the appearance and movements of the feet 
and legs. The feet are greatly enlarged symmetrically in acro- 
megaly and in Marie's pulmonary osteo-arthropathy. In the latter 
disease the enlargement is particularly noticeable because it is the 
extremities which are chiefly hypertrophied, whereas in acromegaly 
there is simultaneous enlargement of the shafts of the long bones. 
(See chapter on the Hands and Arms.) It is to be remembered that 
in both acromegaly and pulmonary osteo-arthropathy the enlarge- 
ment seems to be due to hypertrophy of all the tissues composing 
the foot, whereas, on the other hand, in myxedema the foot, though 
enlarged, is puffed and swollen in appearance through increase 
of the subcutaneous tissues alone. Often the foot appears 
to be a good deal enlarged as the result of deformity, particularly 
that which consists in partial displacement of the articular surfaces 
of the metatarsal and phalangeal bones through the wearing of 
badly fitting shoes, or joint troubles, of which we shall speak later. 

Under the name of " sciopedy" Power has reported a case of 
congenital symmetrical enlargement of the anterior part of the foot 



PARAPLEGIA 89 

not involving the heel. Any enlargement of the legs associated 
with this eondition, he states, is due to hypertrophy of the muscles 
resulting from the effort to lift the feet. 

In some cases of locomotor ataxia flatfoot from loss of the plan- 
tar arch is seen, and various dystrophics of the joints take place 
as the disease progresses. 

The peroneal leg type of progressive muscular atrophy may so 
closely resemble the so-called Aran-Duchenne type of progressive 
muscular atrophy as to defy diagnosis, but, as a rule, the latter 
disease affects the arms first, and sensation is not involved. (Se< 
early part of this chapter on the Hands and Arms.) 

Wasting of the muscles of the inner surface of the foot affecting 
the big toe, and those on the outer side involving the movements 
of the little toe, the interossei and the flexor brevis communis, may 
occur from the neuritis due to locomotor ataxia, and as the plantar 
aponeurosis retracts the toes are rendered immovably flexed; in 
other cases in place of flexion there is strong extension. 

The Joints. — The joints of the lower limbs may be swollen 
from an arthritis arising from many causes, such as septicemia, 
gonorrheal infection, syphilis, acute articular rheumatism, typhoid 
fever, tuberculosis, cerebrospinal meningitis, locomotor ataxia, 
hemiplegia, rheumatoid arthritis (arthritis deformans), acute 
myelitis, Morvan's disease. 

Gonorrheal Rheumatism. — When arthritis is due to gonorrheal 
infection it is generally seen in the knees or ankles, and occur> in 
men as a rule. It is an infectious arthritis and lasts very persist- 
ently, often attacking at the same time joints so rarely involved 
by rheumatism as the jaw, the vertebral joints, and the sterno- 
clavicular articulation. According to the late Dr. Howard, of 
Montreal, it occurs in five forms: 

(a) Arthralgic, in which there are wandering pains about the 
joints, without redness or swelling. These persist for a long time. 

{b) Rheumatic, in which several joints become affected, just as 
in subacute articular rheumatism. The fever is slight; the local 
inflammation may fix itself in one joint, but more commonly 
several become swollen and tender. In this form cerebral and 
cardiac complications may occur. 

(c) Acute gonorrheal arthritis, in which a single articulation 
becomes suddenly involved. The pain is severe, the swelling exten- 
sive and due chiefly to peri-articular edema. The general fever is 
not at all proportionate to the intensity of the local signs. The 
affection usually resolves, though suppuration occasionally super- 
venes. 

(d) Chronic hydrarthrosis. This is usually monarticular, and 
is particularly apt to involve the knee. It comes on often without 



90 THE FEET AND LEGS 

pain, redness, or swelling. Formation of pus is rare. It occurred 
only twice in 96 cases tabulated by Nolen. 

(e) Bursal and synovial form. This attacks chiefly the tendons 
and their sheaths, and the bursa? and the periosteum. The articu- 
lations may not be affected. The bursa? of the patella, the olec- 
ranon, and the tendo Achillis are most apt to be involved. 

Acute Articular Rheumatism. — Acute articular rheumatism in 
the knee or ankle produces swelling of the joint, redness, heat, 
exquisite tenderness, immobility from pain, swelling of the sur- 
rounding tissues. It does not remain for a long period unchanged 
in one joint, is a process accompanied by fever, and usually modi- 
fied by fu.l doses of the salicylates. 

Acute Synovitis. — Acute synovitis is generally the result of an 
injury, is confined to one joint, is often accompanied by far greater 
effusion into the joint than is seen in rheumatism, and there is no 
systemic disturbance. Should a single joint be affected by an 
aberrant attack of acute rheumatism or synovitis not following 
injury, the physician should never forget the possibility of its being 
a syphilitic arthritis. 

Locomotor Ataxia. — The most marked alterations in the 
joints are those produced by advanced locomotor ataxia, and 
are called arthropathies. Often they are associated with sponta- 
neous fractures of the bones. The knees are most commonly 
involved, then the ankles and hips. A joint or several joints may 
become suddenly swollen with or without pain, and without appar- 
ent cause, until the swelling becomes quite massive. There are 
then developed osseous hyperplasia and a tendency to dislocation 
with crepitation on movement, and the ends of the bone become 
worn away and absorbed. Dislocation and fractures are common, 
and the bones are atrophied. 

Rheumatoid Arthritis. — In rheumatoid arthritis there is a gradual 
enlargement of the joints from accumulation of fluid, which in turn 
is absorbed, lea ing the articulating surfaces roughened, uneven, and 
deformed, but there are no deposits of urate of sodium as in gout, the 
deformities being due to alterations in the articulating surfaces them- 
selves, and the peri- articular development of bone. The disease 
always remains in the joint originally attacked, although new joints 
are involved. Pain is often severe, dislocations and fractures are 
rare, and the small joints are often involved. (See chapter on the 
Hands and Arms.) 

Rheumatoid arthritis when it progresses to an advanced stage 
causes great deformity by the locking of the joints through the develop- 
ment of osteophytes. By the destruction of the cartilages, wasting 
of the muscles, and thickening or contraction of the ligaments, it 
may cause dislocation of all sorts, and false positions. In the great 



PARAPLEGIA 9] 

majority of cases it occurs in women between twenty and thirty 
years of age, but it may develop in early childhood. Pain is severe 
in some cases, absent in others. The thighs become flexed upon the 
abdomen, and the leg on the thigh. The number of joints involved 
varies greatly, but the involvement is generally symmetrical. 

Sometimes this disease, which is generally gradual in its onset, 
becomes very acute, speedily involving many joints, causing swell- 
ing of the synovial sheaths and bursa 1 , and being accompanied by 
some febrile movement. The suddenness of its onset, the febrile 
movement when the onset is sudden, and the pain may cause it to 
resemble acute articular rheumatism, but the absence of redness in 
the joints and of the migration of the swelling from one joint to another 
which is the characteristic of acute articular rheumatism, aids in the 
differentiation. The arthritis of acute central myelitis is sudden in 
its onset, generally multiple, and accompanied by the other symptoms 
of that disease. (See Paraplegia and Anesthesia of the Skin. ) 

Arthritis of Cerebrospinal Meningitis is a typical infectious arthritis, 
and the presence of the characteristic signs of the disease renders 
its cause evident. The joints are many of them affected simulta- 
neously with swelling, pain, and serous or purulent effusions. 

Septic Arthritis. — In cases of septic arthritis the joints become 
swollen and often suppurate, so that the articular surfaces become 
more or less destroyed. This may occur after infection during the 
puerperium or in any case of pyemia. Another arthritis, probably 
infectious, is sometimes seen in epidemic dysentery and in scarlet 
fever. Rarely immediately after or some months after typhoid 
fever a hypertrophic osteo-arthritis comes on as a result of a local 
disease produced by the bacillus of Eberth. This is to be separate* 1 
from ordinary septic arthritis following typhoid fever. 

Acute Osteomyelitis. — The onset of an inflammation in the lower 
end of the femur or in the upper end of the tibia, producing what, at 
first glance, seems to be an arthritis and sometimes simultaneously 
involving other areas near joints, should raise a suspicion of acute 
osteomyelitis, which is a fatal disease in many cases unless surgical 
aid comes to the patient. The symptoms consist of boring pain in 
the part, great tenderness and swelling, and the skin soon breaks down 
as a purulent and offensive discharge makes its way to the surface. 

Closely allied to this is the acute epiphysitis of infancy, in which 
there is suddenly developed a chill followed by great pain and swell- 
ing of the joints or their neighborhood. The skin becomes engorged 
with blood and the joint fills with pus. Care must be taken to sepa- 
rate this condition from rheumatism and the joint swelling sometimes 
seen after typhoid fever and that form which is due to infantile scurvy. 

Subperiosteal Hematoma. — Great swelling of the thigh or leg 
occurring in a child may be due to subperiosteal hematoma 



92 THE FEET AND LEGS 

(Moller-Barlow's disease). Aspiration of the swelling will reveal the 
character of its contents, and the fact that the child is usually a 
sufferer from rickets will aid in the diagnosis. 

Gout. — Although gout is capable of causing deformity in the lower 
extremities, it has one fact about it which is of practical importance, 
namely, that it involves the small joints of the foot, while rheumatism 
attacks the large joints, such as the knee, by preference. Gout 
involves the feet most commonly, the big toe being the favorite place 
for gouty manifestation, whereas rheumatism is more frequently seen 
in the hand, if small joints are affected. Aside from the swelling, red- 
ness, and exquisite tenderness of gouty joints, all of which symptoms 
exceed in acuteness, if possible, similar manifestations in acute rheu- 
matism, there is often an additional and permanent cause of deformity 
in the chalk stones which are deposited about the joints, and which 
are never seen in rheumatism. The history of frequently recurring 
attacks lasting but a few days, accompanied by enlargement of the 
veins about the joint and shedding of the skin locally, points, when 
added to the symptoms named, to a typical case of gout. In chronic 
cases it may be almost impossible to determine whether a case be 
one of chronic rheumatism or gout unless chalk deposits can be 
found. (See chapter on the Hand.) 

Sometimes in chronic lead poisoning we have developed what is 
known as plumbic gout, owing to the deposition about the joint of 
urate of lead and sodium. 

Dengue. — The onset of a multiple arthritis, with which there are 
headache, chills, intense aching in the bones, joints, and muscles, 
and a fever rising as high as 106° or 107°, and rarely an erythematous 
rash, may indicate the presence of dengue. The joints are swollen 
and painful, and often both the large and small ones are involved. 

In Schbnlein's Disease, which is a form of very severe purpura, 
multiple arthritis, with great pain, and purpuric eruptions occur 
and the presence of the subcutaneous exudate with edema and 
sloughing of the mucous membrane of the mouth adds to the pic- 
ture. The patient seems very ill, but death rarely follows. Such 
cases are rare, but the writer saw one in consultation with Dr. 
Wilson, of Woodbury, New Jersey, in which alarming sloughs of 
the tonsils and buccal mucous membrane occurred in addition to 
the arthritis changes. (See chapter on the Skin.) 

Very nearly allied to this are the joint involvements of hemo- 
philia, which in their sudden onset and pain closely resemble rheu- 
matism, particularly as the large joints are commonly involved. The 
history of the patient being a bleeder, or of his being related to one, 
may clear up the diagnosis. 

Spontaneous Dislocation of the Hip. — So-called spontaneous dislo- 
cations of the hip have been recorded during convalescence from 



PARAPLEGIA 93 

typhoid fever, scarlet fever, and acute rheumatism. The luxation 
in the latter disease usually follows severe pain, and the ligaments 
are often found torn from their attachments. In typhoid and 
scarlet fevers the dislocation occurs insidiously and announces itself 
by the pain it causes. 

Intense Swelling.— Intense swelling of the leg, aside from that due 
to ordinary edema, may be due to milk leg, which is a condition of 
swelling of the entire limb, generally limited to one side, and seen 
during the puerperium or after any one of the infectious fevers, 
such as typhoid. The joints are not particularly affected. On the 
contrary, the calf of the leg is the part most affected, it being white, 
firm, hot, but slightly, if at all, edematous. Pain is excessive, there 
is entire loss of power in the affected limb, and its temperature is 
much higher than normal. 

If the swelling of the leg is bilateral and pits on pressure, it is 
practically always the result of anasarca from renal or cardiac dis- 
ease; but if unilateral, it may be, as just stated, due to thrombosis 
of the femoral vein. (See chapter on the Skin; Edema.) 

Gangrene. — Three very important and serious alterations in the 
nutrition of the foot remain to be noted, namely, perforating ulcer 
due to tabes dorsalis, diabetic gangrene and senile gangrene. 

Perforating ulcer usually appears in one foot, beginning with the 
formation of a bleb, which changes to an abscess, which in turn is 
followed by necrosis of all the tissues of the foot immediately under- 
lying the destroyed skin. With it are associated the signs of ataxia. 
Sometimes perforating ulcer of the foot occurs during the course of 
diabetes mellitus, but it is probable in many such cases that loco- 
motor ataxia is associated with diabetes. 

In diabetic gangrene the toes are nearly always affected in prefer- 
ence to other parts of the body. An analysis of the urine will 
aid the diagnosis. (See chapter on the Skin.) 

In senile gangrene the age of the patient, the presence of bad blood- 
vessels, and the absence of a sufficient cause for gangrene, as, for 
example, trauma, separate the case from any other condition, while 
the additional facts that senile gangrene generally affects the inner 
side of the foot, especially the big toe, and is a dry gangrene, render 
the diagnosis easy. 

Gangrene of the lower extremities sometimes follows the infectious 
diseases, such as scarlet and typhoid fevers, 1 from thrombosis of 
the femoral artery. It may also occur in the course of exophthalmic 
goitre. 

More rarely gangrene of the foot and hand follows embolism due 
to cardiac valvular disease. It is extremely painful, and septic 
fever may ensue. 

i See "The Medical Complications and Sequela' of Typhoid Fever," by the author. Lea 
Brothers & Co., Philadelphia, 1899, 



94 



THE FEET AND LEGS 



Mycetoma. — In this connection mention may be made of 
"Madura foot/' or mycetoma, a chronic local disease of tropical 
climates, and called "fungus foot disease" in India. A small tumor 
develops on the foot or hand, which, after the lapse of twelve to 
twenty-four months, bursts and leaves several sinuses from which 
escape black particles or whitish-red bodies like fish-roe. The dis- 
ease may spread up the leg. The pale particles in the discharge look 
like actinomyces. 




Fig. 31. — Testing the knee-jerk with the percussion hammer. 

Ainhum. — Ainhum is a disease peculiar to dark-skinned races, 
characterized by gradual drying up and separation of the toes (by 
a constriction), usually the little toe. It has been thought to be 
related to leprosy, but this is doubtful. 

Periosteal Thickening. — Alterations in the appearance of the 
tibiae or shins often give us a clear idea of the presence of late 
syphilis, either because of gummatous swellings in this neighbor- 
hood or owing to the development of periosteal thickening and 
exostoses. 



PARAPLEGIA 



95 




Fig. 32. — Testing t he knee-jerk by a blow with the ulnar edge of t lie hai 




Fig, 33. — Testing the knee-jerk by means of the percussion hammer, the patient being 

recumbent. 



96 



THE FEET AND LEGS 




Fig. 34. — Testing ankle clonus with the patient recumbent. 




Fig, 35, — Testing ankle clonus when the patient is seated, 



PARAPLEGIA 



97 



Physical Methods Employed in Examining the Feet and Legs. 
The Knee-jerk. — The method of testing the knee-jerk consists in 
seating the patient on a chair of ordinary height, instructing him to 
cross his legs in the position which he would occupy if sitting at 
ease, and then to sharply tap the tendon of the knee-cap, between 
the patella and its insertion into the tibia, by means of a rubber 
hammer or with the ulnar edge of the hand. (See Figs. 31 and 32.) 




Fig. 36. — Testing the " station." Eyes closed; feet close together. 

When the patient is too weak to sit up, the lower limb may be 
elevated from the bed so that the thigh and leg are at an angle 
of about 45 degrees, the lower third of the thigh resting on the 
left hand of the physician in such a way that the leg hangs supine. 
(See Fig. 33.) 

Ankle Clonus. — This test can be made when the patient is seated 
or recumbent. When recumbent the examiner grasps the leg near 
7 



98 THE FEET AND LEGS 

the knee with the left hand in order to support it. He then extends 
the leg on the thigh with the right hand, grasping the ball of the foot. 
When the limb is in this position, the leg being well extended on the 
thigh, the foot is flexed sharply toward the knee and immediately 
released from pressure. (See tig. 34.) If clonus is present, the foot 
will undergo a series of coarse, tremulous movements in extension and 
flexion. 

Another method of testing clonus is to seat the patient in a chair 
with the leg resting on the ball of the foot on the floor, and then to 
apply sudden pressure, which is quickly relieved, to the knee, when, 
if clonus is present, the limb undergoes a series of tremulous up-and- 
down movements. (See I ig. 35.) 

Station. — This is determined by having the patient stand with his 
feet close together and then directing him to close his eyes, or if he 
cannot be relied upon to completely close his eyes, to blindfold him. 
(See Fig. 36.) A normal patient should stand almost perfectly 
steadily under these circumstances, but in several diseases, notably 
locomotor ataxia, he will sway very greatly, or even fall. 

The Cremasteric Reflex. — This reflex consists in a retraction of the 
testicle and scrotum upon irritating the skin upon the inner surface 
of the thighs. For methods of testing the various conditions of 
sensibility in a limb, see chapter on the Skin. 



CHAPTEE IV. 

HEMIPLEGIA. 

Having considered the manifestations of disease as seen in the 
arms and legs in connection with monoplegia and paraplegia, spasm 
and contracture, we must now study the diagnostic meaning of hemi- 
plegia, or that form of paralysis which involves the arm and leg and 
head on one side of the body. This form of paralysis, when com- 
plete, is always due to a lesion arising above the spinal cord — that 
is, in the brain, and is due to lesions in the lower tracts of the 
brain or in its cortex. The character of the paralysis, the association 
of other symptoms wit 1) it, and the history of the patient and of his 
illness will render a diagnosis easy as to the approximate site of the 
lesion in most cases. The most common causes are hemorrhage 
into the cerebral tissues from a ruptured bloodvessel, or embolism 
or thrombosis of some vessel supplying important areas. Still other 
causes of hemiplegia are brain tumors, meningeal hemorrhage, 
degenerative processes, and hysteria. 

Before we enter into consideration of the various symptoms 
resulting from central nervous lesions it is well to stop for a moment 
for the purpose of clearly understanding the anatomy and physiology 
of the parts involved, in order that we can properly study the results 
of lesions in the nerve centres or nervous tracts. 

It is not necessary to remind the reader that the brain is divided 
into three areas, the frontal area being concerned with intellection, 
the middle area with motion, and the posterior area with sensation 
and special sense. These areas are again divided into subareas, 
each of which governs or is connected with several functions, and 
still further subdivisions exist, in which reside the centres governing 
small areas, as, for example, a single muscle or group of muscles. 
(See Fig. 37.) Disease of any part of the brain surface, therefore, 
modifies more or less the function of that part and the part of the 
body tributary to it. Beneath the surface, through the so-called 
white matter, various fibers pass, which carry to or from the centres in 
the cerebral cortex the impulses connected with their function, and 
these fibers approximate one another more and more closely in the 
lower part of the brain until they form a bundle (the corona 
radiata). Thus we see in Fig. 37 how the fibers arising from 
the middle area of the cortex cerebri pass down through the 



100 



HEMIPLEGIA 



t0 WEK 




Fig. 37.— Diagram showing the fibers from the cortex forming the corona radiata, which 
after they are approximated pass into the internal capsule. It also shows the decussation of 
the pyramid of the left side, which passes to the right side of the spinal cord, and the direct 
or uncrossed tract (Tiirck's column). Finally it also shows the secondary degeneration which 
occurs after cerebral hemorrhage or softening, and which follows the course of the motor 
tracts into the spinal cord. H. Site of lesion. The continuous lines are fibers going to the 
legs, the dotted are those going to the arms and motor cranial nerves. (Modified from Van 
Gehuchten.) 



HEMIPLEGIA 



101 



lenticular nucleus into the knee or angle of what is called the internal 
capsule. These fibers are arranged in such a way that those 
arising from the lower part of the cortex, as in the face center, lie 
nearest the knee of the capsule, and those highest, farthest from 




Fig. 38.— Cross- section of the brain, showing the lateral ventricles, the cerebellum, and, 
most important, the cross-section of the motor fibers in the internal capsule. (Modified from 
Fuller.) 

this point (Fig. 38). After the motor fibers have passed through 
the internal capsule they pass into the cms cerebri of that side, which 
(the cms cerebri) connects the hemisphere of the same side with the 
cerebellum behind it, and the pons and medulla below it. The crura 



102 



HEMIPLEGIA 



cerebri are two thick, cylindrical bundles of white matter which 
emerge from the anterior border of the pons (see Plate II), diverge as 
they pass upward and outward to enter the under part of each hemi- 
sphere, as if stretching out to receive the motor fibers from the inter- 
nal capsule. From the crura cerebri the motor fibers pass downward 



Lesion of cerebral mo- 
noplegia {.brachial) 



Lesion of ordinary 
hemiplegia 



Lesion of cross paralysis 
(face of same side with 
limbs of other side) 



A lesion causing paraplegia 



A lesion causing hemi- 
paraplegia 




Cortical centre for op- 
posite leg 



Cortical centre for op- 
posite arm 



Cortical centre for op- 
posite side of face 



Internal capsule (pos- 
terior limb) 



Motor nerve to face 



Decussation of pyra- 
mids 



Crossed pyram idal tract 



Motor nerves to upper 
limb 



Crossed pyramidal tract 



Sensory nerves entering 
cord, and decussating 
soon after entry 



Motor nerves to lower 
limb 



FIG. 39. 



-Diagram showing the general arrangement of the motor tract and the effect of 
lesions at various points. (Ormerod.) 



into the pons Varolii. Here the fibers which have hitherto travelled 
together divide into two parts, namely, those from face and tongue 
centre, which pass to the opposite side and become connected with 
the nuclei of the facial and hypoglossal nerves, which act as minor 
centres governing the face and tongue, and the fibers for the arm, 
leg, and trunk of the body, which continue on down to the medulla 



PLATE II 




Base of the Brain, showing the Cranial Nerves. 

The crura cerebri are seen on either side of the posterior perforated space and under the third 
nerves. The various cranial nerves are numbered with Roman numerals. (Modified from Arnold.) 



HEMIPLEGIA 



103 



oblongata, where they form the so-called pyramids, and having done 
so most of the fibers cross to the opposite side of the spinal cord 
(the crossing of the pyramids), and so form the crossed or lateral 
pyramidal tracts. (See Fig. 37.) A smaller number of fibers, how- 
ever, pass directly down to the spinal cord from the medulla oblon- 
gata, and form what is called the direct or anterior pyramidal tract. 
Direct, because it does not cross; anterior, because it lies along the 




Fig. 40. — Showing the mechanism of different hemiplegias. A les-ion at A causes complete 
hemiplegia by destroying the motor tract. One at M causes paralysis of third cranial nerve 
(motor oculi) by destroying its nucleus or root on same side, and paralysis of arm and leg on 
opposite side. A lesion at F causes facial palsy on same side, hemiplegia on opposite side. In 
a lesion at H the hypoglossus would be affected on one side, with hemiplegia on the other. 
(Modified from Edinger.) 

edge of the anterior fissure of the cord; pyramidal, because it comes 
down from the pyramid. This is sometimes called Tiirck's column. 
(See Fig. 37.) It is by means of these two tracts in the spinal cord 
that motor impulses pass down to the nerve trunks and muscles. 

We can understand, therefore, that if a small lesion occurs at the 
peripheral endings of the corona radiata — that is, on the cerebral 



104 



HEMIPLEGIA 



cortex — it will only produce a limited paralysis. Thus, as seen in 
Fig. 37, a clot at the arm centre would only involve the arm fibers. 
If, however, the lesion be lower down where the fibers of the corona 
radiata are getting closer and closer, as, for example, in the internal 
capsule, then even a small lesion will produce widespread paralysis, 
since it will involve a large number of fibers running ultimately to 
widely separated areas in the body, and, if large enough, produce 
hemiplegia. (See Fig. 37, lesion H, and Fig. 40, lesion A.) If the 
lesion be situated in the pons on one side, it will cause facial paralysis 
on that side and hemiplegia on the opposite side of the body, because, 
as shown in the diagrams (Figs. 39 and 40, M), it will, under these 
circumstances, destroy the facial fibers after they have crossed, and 
the remaining motor fibers before they cross. The various tracts, 
motor and sensory, in the spinal cord are shown in Fig. 41. 




Fig. 41. — Showing the various tracts in the spinal cord on cross-section. 
(Nervous Diseases, Mills.) 

Hemiplegia from Hemorrhage is characterized by sudden onset 
in most cases, by more or less mental disturbance and disorders of 
motion, sensation, and of the special senses according to the site 
of the leaking vessel. The skin reflexes are apt to be markedly 
decreased and the deep reflexes increased, but the bladder and rectum 
are not usually paralyzed, although in the first shock of the accident 
there may be vesical and rectal incontinence. The mental dis- 
turbance usually amounts to a rapidly oncoming unconsciousness 
in hemorrhagic hemiplegia. 



HEMIPLEGIA FROM HEMORRHAGE 



105 



The question of the location of the lesion is very important. In 
the great majority of cases it is situated above the point at which 
the decussation of the motor fibers takes place in the medulla, and 
is, therefore, on the opposite side of the body from that on which 
the hemiplegia exists. If, however, the lesion be below the decus- 
sation, the paralysis and lesion are on the same side, as just de- 
scribed. The most common site for the lesion in hemiplegia is in the 
knee or posterior limb of the internal capsule, owing to the fact that 
the middle cerebral artery in one of its lenticulo striate branches 
perforates the internal capsule, and ends in the caudate nucleus, and 
this artery is so commonly ruptured that Charcot has called it the 
"artery of cerebral hemorrhage" (Fig. 42). If the hemorrhage 
does not involve the posterior third of the internal capsule, there 
are no sensory symptoms associated with the motor loss, but the 




Fig. 42. — Showing distribution of bloodvessels to internal capsule. Tbe artery marked x is 
the so-called artery of cerebral hemorrhage, and it is readily seen how its rupture destroys the 
fibers in the internal capsule. (Modified from Gordinier.) 

paralysis will be practically universal on that side, involving the 
leg and arm, and the lower part of the face, so that the mouth is 
drawn toward the healthy side. (Explained by Fig. 38.) The symp- 
toms associated with hemiplegia dtie to this cause often become very 
severe, because the hemorrhage is so profuse that the lateral ven- 
tricle becomes filled with blood, and from it the blood passes to the 
third and from there to the fourth ventricle, where, by pressure 
on the vital centres, it speedily produces death. In such cases deep 
unconsciousness, stertorous breathing, a slow, full pulse, and a 
flushed skin, becoming somewhat cyanotic, may be present. Re- 
covery never occurs, for the secondary inflammation, or softening, 
following the outflow of blood produces fatal results, even if the 
patient survives for some days 

In cases in which the hemorrhage is very limited consciousness 
may be lost for only a brief period, and at most there may be only 



106 HEMIPLEGIA 

mental confusion. Often in mild cases there is a slight return of 
power in the affected side within a few days, and the temperature 
of the affected part, which has been raised, approaches the normal. 
Finally, after six to eight weeks, the dominant symptoms consist in 
partial loss of power of the arm and leg, and the facial paralysis 
has perhaps entirely disappeared, although the tongue when pro- 
truded may tend to go over to one side. If the case does not pass 
to such favorable results, instead of recovery of power at this time 
there are developed contractures and secondary rigidity from degen- 
erative processes extending to the pyramidal tracts. (See Fig. 37.) 
Hitzig has shown that these conditions are apt to be least marked 
in the morning. Wasting of the paralyzed muscles only ensues 
from the disuse and not from true trophic change. 

When the case is not of the very severe type which causes death 
in a few hours, and yet the lesions are such that recovery is not 
going to take place, the patient at the third or fourth day becomes 
unconscious a second time, his temperature rises, he mutters, and 
grows restless, finally becomes comatose, then develops respiratory 
failure, or a hypostatic congestion of the lungs, and dies. 

When a patient is seized with headache, dizziness, vertigo, and 
vomiting, and rapidly oncoming hemiplegia and hemianesthesia, 
attended at first with no loss of consciousness, but in a day by un- 
consciousness and coma, he is suffering from what has been called 
"ingravescent apoplexy." The hemorrhage, under these circum- 
stances, begins in the knee of the internal capsule, proceeds back- 
ward until it involves the sensory fibers in the internal capsule, and, 
finally, breaks into the lateral ventricle, soon after which death 
ensues. 

When a hemiplegia is followed by rigidity very early, with sen- 
sory involvement and convulsions, the lesion is probably cortical, 
or, more correctly is secondarily cortical to a deeper hemorrhage, 
and spreads over the centres for the face, arm, and leg. Most 
commonly, cortical hemorrhages are due to injuries, although they 
may arise from unprovoked vascular rupture. In any case, they 
are usually ushered in by convulsions. (See next page.) 

If in the development of symptoms of cerebral hemorrhage there 
be little hemiplegia and temporary unconsciousness, followed in 
some hours by a sudden aggravation of the symptoms, it may be 
that in the beginning of the attack the lesion has been in the frontal 
lobes, but has gradually extended backward until it has ruptured into 
the lateral ventricle. So, too, a hemorrhage into the occipital lobe 
or the posterior part of the parietal lobe is rarely marked by much 
hemiplegia, and, if present, the leg is more paralyzed than the arm. 
A characteristic symptom of this lesion is, however, well-marked 
hemianesthesia (see chapter on the Skin) and hemianopsia. (See 



PLATE III 




Showing the Area of the Middle Meningeal Artery, in the Inner Table of the Skull, Injury 
to which is Sometimes the Cause of Hemiplegia. (Arnold's Atlas.) 



PLATE IV, 




The same Artery with the Inner Table of the Skull Removed. (Arnold's Atlas.) 



HEMIPLEGIA FROM HEMORRHAGE 107 

chapter on the Eye.) Generally, however, such changes result from 
a thrombosis. 

Hemiplegia developing after an injury to the head is usually due 
to rupture of the middle meningeal artery or one of its branches. 
(See Plates III and IV.) Owing to the fracture of the skull, the vessel 
is ruptured. A pathognomonic sign of this accident is the fact that 
there is a period of consciousness between the time of injury and the 
development of unconsciousness. The patient may be momentarily 
stunned, then recover consciousness, and then relapse into a second 
period of unconsciousness which rapidly deepens into profound 
coma. It is important to remember that while the paralysis is on 
the opposite side of the body from the hemorrhage, the hemorrhage 
may be on the opposite side from the external injury, since the 
fracture of the skull may be a fracture by contre-eoup. The paralysis 
is usually progressive from part to part, and convulsions may occur 
as a result of cortical irritation produced by the hemorrhage. A 
wide dilatation of the pupil on the side of the hemorrhage 
("Hutchinson's pupil") may be present. Such a hemorrhage is 
said to be supradural. Sometimes the hemorrhage arises from the 
ascending frontal or ascending parietal artery, and is then subdural 

The following table, from Mills' Nervous Diseases, gives the 
differentiation between ventricular and meningeal bleeding: 

Ventriculctr Hemorrhage. Meningeal HemorrK 

No antecedents to explain the lesion. Antecedents: for the newborn a pro- 

longed or hard labor; for the adult a 
traumatism. 
Premonitory symptoms not rare. Premonitory symptoms generally absent. 

Gradually deepening unconsciousness. When traumatic, unconsciousness tal- 

lowed by partial re>toration of con- 
sciousness and then again by uncon- 
sciousness. 
Cephalalgia rare. Cephalalgia frequent 

Paralysis when present is usually hemi- Paralysis ordinarily generalized; hemi- 

plegic. plegia exceptional. 

Varying pupillary conditions. Unilateral dilatation of pupil common. 

Deviation of the mouth and tongue very Deviation of the mouth and tongue rare. 

common. 
Contractures very common. Contractures, although frequent, less 

common. 
Convulsions may be present, but not Convulsions the rule. 

common. 
Vomiting not frequent. Vomiting frequent. 

No symptoms of secondary meningitis Symptoms of secondary meningitis with 
with fever. high fever toward the third or fourth 

day. 
Death rapid. Life, as a rule, prolonged several days. 



108 HEMIPLEGIA 

When there is developed in cases of hemiplegia, aphasia or dis- 
ordered speech, there is probably a lesion in the neighborhood of 
the third frontal convolution, or the island of Reil. (See chapter on 
Speech.) 

Hemiplegia may be due to cerebellar hemorrhage, in which case 
there are loss of consciousness deepening into profound coma, con- 
tracted pupils, vomiting in many of the cases, and finally death 
when hemorrhage breaks into the lateral ventricle. The diagnosis 
of cerebellar hemorrhage is very difficult. 

Of the irregular forms of hemiplegia there are several. Some- 
times the leg is from the beginning more affected than the arm, and 
remains paralyzed long after the face and arm have recovered. The 
leg may become rigid and distorted by contractures, and there will 
often be found present marked anesthesia of the skin of the paralyzed 
leg and arm, with hemianopsia and aphasia. Such symptoms indi- 
cate a lesion of comparatively small size involving the leg fibers 
and some of the sensory fibers in the internal capsule, and result 
from rupture of the lenticulo-optic artery. When the arm suffers 
most the symptoms just described as occurring in the leg are found 
in it, and motor aphasia, if the lesion is on the right side, is often very 
marked, as is also facial paralysis. This is supposed to be due to the 
anterior frontal artery, a branch of the inferior anterior cerebral 
artery, becoming diseased. 

When posthemiplegic chorea attacks the paralyzed limbs there 
is often a focal lesion in the posterior extremity of the internal 
capsule. 

Embolism and Thrombosis. — The symptoms which have just 
been detailed may also arise, as already said, from embolism 
or thrombosis of the cerebral vessels. How are we to separate 
the hemiplegias of hemorrhage and occlusion? In many cases 
this is impossible, but there are some differential points which 
may aid us. In the first place, thrombosis is a condition of 
advanced age, while hemorrhage may occur at any time from 
thirty years of age on. The presence of hemiplegia in a young 
man, therefore, is probably not due to a thrombosis. Again, hemor- 
rhage occurs often after exertion or the drinking of stimulants, and 
occurs rarely in sleep, whereas thrombosis not rarely comes on under 
these circumstances, and often develops during the night, so that 
the patient awakes paralyzed, but a patient may have both throm- 
bosis and apoplexy. In hemorrhage, consciousness is generally 
lost, whereas in thrombosis it is often only dimmed. Vomiting and 
contracted pupils from pressure on the lower centres indicate hemor- 
rhage, while their absence may point to thrombosis. Finally, the 
general systemic shock and febrile movement are apt to be greater 
in hemorrhage than in thrombosis. The history of syphilitic infec- 



ADDITIONAL CAUSES OF HEMIPLEGIA [09 

tion, producing an endarteritis, also points to thrombosis, although 
hemorrhage may arise from this cause also. 

The diagnosis of embolism producing hemiplegia from the par- 
alysis due to hemorrhage is always more or less difficult, but the 
presence of chronic or ulcerative endocarditis or their results, or other 
cause for the formation of emboli, aids the diagnosis. Where the 
cause is embolism the onset is sudden, whereas in thrombosis it is 
sometimes more gradual. The paralysis from embolism is more 
commonly on the right side of the body, owing to the fact that it 
is more easy for an embolus to pass into the left middle cerebral 
artery than into the right. 

Additional Causes of Hemiplegia. — Spastic hemiplegia may be 
due to cerebral tumor, and is often associated with convulsions, 
particularly if the growth be cortical. Very often the paralysis of 
cerebral tumor will be found, from the history, to have come on 
gradually. Thus, the history may be that at first the side of the 
face has been paralyzed, then the arm and then the leg, and that the 
complete loss of power has not been sudden but gradual in the pail 
affected, or that a convulsion has left that side, which was pre- 
viously only impaired in strength, totally paralyzed. 

Hemiplegia also comes on as a result of cerebral syphilis, and, 
aside from a history of specific infection and response to specific 
medication, presents few characteristic signs. The presence of 
intense headache, convulsions of an epileptiform type, and the fact 
that the paralysis occurs in some cases in early adult life, point to 
its origin. 

Another cause of hemiplegia is diffuse cerebral sclerosis of one 
hemisphere (not multiple sclerosis), in which the most constant 
symptoms are, in addition to the paralysis, evidences of motor irri- 
tation, such as epileptoid convulsions of a bilateral or unilateral 
character, rhythmical or arhythmical twitchings of the muscles like 
chorea, and dementia. 

Hemiplegia arising from acute infantile cerebral parali/sis has 
many of the distinctive features already described when discussing 
the paraplegia due to this diseased state. The age of the patient, 
the occurrence of epileptiform convulsions and of athetosis in the 
affected parts, and the patient's history are the important points to 
be recalled in making a diagnosis. The lesion is always due to a 
cerebral hemorrhage or to embolic softening. 

When hemiplegia occurs in locomotor ataxia, it depends not upon 
the disease, but upon a complicating hemorrhage, embolism, or 
thrombosis. 

A slowly developed hemiplegia sometimes results from dissemi- 
nated sclerosis, the pathological process involving the side of the 
pons and spinal cord ; but the intention tremor, the peculiar speech, 



110 HEMIPLEGIA 

the nystagmus, and the very excessive reflexes aid us in the diag- 
nosis of their cause of the loss of power. (See chapter on the Hands 
and Arms, part on Tremor.) 

A form of hemiplegia which is often very misleading is that 
occurring in general paralysis of the insane or paretic dementia. 
In this disease the patient often has attacks of vertigo, unconscious- 
ness, and more or less marked hemiplegia or monoplegia, sometimes 
with aphasia if the right side is paralyzed. This form is also liable 
to be wrongly diagnosticated by reason of the epileptiform convul- 
sions, which frequently occur, and which in connection with the 
paralysis give the impression in the first attack that there is a 
hemorrhage of the cerebral cortex. The altered disposition of the 
patient, the loss of memory and intelligence, the peculiar stumbling 
speech, and the curious changes in the handwriting are some of the 
symptoms which complete the diagnostic picture. 

In this condition we should not forget the possibility of hemiplegia 
or monoplegia occurring with suddenness in the course of renal 
disease producing uremia The paralysis may be permanent or only 
transient, but the urine will be found to be albuminous, and the 
other signs of renal disorder may be manifest. 

Hemiplegia sometimes comes on in purulent meningitis. The 
history of a head injury or of a pyemic or infective process, the 
cerebral symptoms, the stiffness of the back of the neck, the impair- 
ment of the normal movements of the eyeball, and the optic neuritis, 
associated with the convulsions, make the diagnosis possible. 

Crossed Paralysis. — When there is paralysis of the arm, trunk, 
and leg on one side, with facial paralysis and anesthesia on the 
opposite side of a well-marked type, associated with early rigidity of 
the paralyzed side, conjugate deviation of the eyeballs, a very marked 
rise in bodily temperature, a contracted pupil, and convulsions, with 
difficulty in swallowing and in speech, the lesion is to be found in 
the pons Varolii on the side opposite the paralysis. This is due to 
the fact that the injury is below the decussation of the facial nerve. 
(See Figs. 30 and 31.) If both sides of the face are paralyzed, with 
hemiplegia elsewhere, the lesion is in the pons where the facial 
fibers cross. Pons paralysis is nearly always associated with gid- 
diness, vomiting, conjugate spasm with nystagmus, albuminuria, 
glycosuria, and marked disturbances in the respiration and heart. 
Pontile hemorrhages are, however, very rare, and usually are rapidly 
fatal. 

If in a case of hemiplegia there is not only paralysis of the arm 
and leg and of the lower part of the face on one side, but in addition 
paralysis of the upper part of the face on the opposite side with 
ptosis on that side due to paralysis of the facial and oculomotor 
nerves, and with these symptoms impaired sensibility and vasomotor 



CROSSED PARALYSIS HI 

changes in the limbs, the lesion is probably in the crus cerebri on 
the side of the upper facial paralysis — that is, on the same side as 
the ptosis. This is only true if the two paralyses have been simul- 
taneous in occurrence, as it is possible for two lesions occurring at 
different times and at different places to produce paralysis of the 
face on one occasion and hemiplegia on another. (See Ptosis in 
chapters on the Face and the Eye.) 

A very rare form of paralysis, in which the arm on one side and 
the leg on the other side are involved, is due to a bulbar lesion just 
where the decussation of the pyramids takes place. This is one of 
the forms of crossed paralysis, and is due to cutting off of one set of 
fibers before they cross, and the others after they have crossed. (See 
early part of this chapter and chapters on the Hands and Arms, 
Feet and Legs, and Face and Head for further information as to 
crossed paralysis.) 



CHAPTER V. 

THE TONGUE, MOUTH, PHARYNX, AND ESOPHAGUS! 

The general appearance of the tongue — Its coating — Its appearance in 
poisoning — Fissures and ulcers of the tongue— Eruptions on the tongue — 
Atrophy and hypertrophy of the tongue — Paralysis — Tremor and spasm 
of the tongue — Tonsillitis — Diphtheria — Pharyngitis — Disease of the 
esophagus. 

THE TONGUE. 

The appearance of the tongue is recognized as indicative of the 
general condition of the patient, and is a valuable diagnostic aid in 
many diseases other than those associated with disorder of the 
gastro-intestinal mucous membrane. In examining this organ the 
physician should take note of the condition of its surface, its shape 
as it lies in the mouth or is protruded, and the character of its move- 
ments. He should also see that it is well protruded, and examine 
the back of it more than the tip, as the latter is the part giving the 
least information. 

Before discussing the precise appearance of the tongue in the 
various disorders in which it becomes altered in appearance it is 
well to remember that its surface is covered by mucous membrane, 
which differs in various parts. The epithelium is scaly and rests 
upon the corium or mucosa. The mucosa also supports many 
papillae, which are thickly distributed over the anterior two-thirds 
of the tongue on its upper surface. These papilla? give the peculiar 
roughness which is so characteristic of this surface, and occur in 
three forms, namely, the circum vallate or large papillae, the fungiform 
or mediate, and the filiform. The circumvallate are only eight or 
twelve in number, and are arranged at the back of the tongue in the 
shape of the letter V, with the point toward the root of the organ. 
The fungiform papillae are scattered freely over the tongue, mostly 
at the sides and tip, and appear as deep-red eminences, the bases of 
which are smaller than their free extremities. Their epithelial 
covering is very thin. The filiform papillae, which cover the ante- 
rior surface of the tongue, are very minute, and arranged in lines 
corresponding in direction with the two rows of the circumvallate 
papillae. From their apices project many fine, filiform processes 
which are of a whitish tint, owing to the density of the epithelium 



THE TONGUE 113 

of which they are composed. There are, in addition, many simple 
papillae which cover the surface between the peculiar ones already 
described. The fungiform papillae are those seen most commonly 
in cases of disease, for they become large and prominent, and 
because of their red color show through the coating as red dots. 

The appearance of the surface of the tongue varies greatly even 
in health according to the condition of its mucous membrane and 
the epithelium covering it. The most common alterations in its 
appearance are due to mere superficial coatings or fur, which consist 
of dead epithelial cells, microorganisms of many kinds, and abnor- 
mally shaped living epithelium. Small particles of food may also 
be present. Butlin believes that the coating is chiefly due to micro- 
organisms. The question as to how characteristic of a particular 
disease any one coating or fur may be has been warmly discussed. 
Some have gone so far as to assert that the coating of the tongue is 
not indicative of any state in particular, while others, of whom the 
author is one, are convinced that, while an absolute diagnosis of 
disease in other organs cannot be based upon the appearance of the 
tongue, great aid can be gained by its study. 

There are, however, very few conditions of the coating of the 
tongue which are pathognomonic of any one disease, since the coat- 
ing is produced by the local conditions of the mouth rather than by 
the disease itself. 

Taking up for consideration the various forms of coating, we find 
that the area at the base between the circumvallate papillae is always 
somewhat coated even in the best of health, and that in disease the 
heaviest coating is generally found in this region, while the tips and 
sides, even in those diseases in which the coating is heaviest, are 
generally fairly clean. This is in part due to the character of the 
epithelium in different parts, and to the fact that the tip and sides 
are generally scraped clean by the movements of the tongue. Fur- 
ther, it should be remembered that the development of coating, 
aside from digestive derangements, depends chiefly on three factors : 
First, immobility of the tongue, so that it is not kept clean by rub- 
bing; second, mouth breathing, w r hereby the surface becomes dry 
and less easily cleansed; and, third, fever, which not only dries 
the surface of the tongue, but interferes with salivary secretion. 
Additional local causes are a decayed or ragged tooth or follicular 
tonsillitis, which infects the lingual epithelium, lack of cleanliness, 
and habits, such as smoking. In the last class of patients, the 
smokers, a heavily coated tongue in the morning is very common. 

The tongue of the typhoid state, and of typhoid fever in parties 

lar, is quite characteristic, because the prolonged illness, the great 

exhaustion, and the general apathy of the patient all conspire to 

produce a peculiar coating on this organ. Early in the disease the 

8 



114 THE TONGUE, MOUTH, PHARYNX, AND ESOPHAGUS 

surface of the tongue may be more or less foul, resembling the coat- 
ing associated with biliousness, in that the back part is coated evenly 
and with a paste; but very soon a characteristic sign appears, namely, 
that the tip of the tongue and its edges become red, and the coating 
becomes most marked on each side of the median fissure, which 
increases in depth from before backward. The tongue also becomes 
narrow instead of broad and flabby, as it is in biliousness, and is 
drier. If the attack be mild, this condition may remain until con- 
valescence is established ; but if the disease runs a severe course, the 
coating becomes very heavy, more dry, rough and brown from ex- 
posure to air and medicine. The furred appearance becomes almost 
shaggy at the back portion, and the drying proceeds until the under- 
lying epithelial layer is cracked and fissured, so that tiny exudations 
of blood add to the lingual discoloration. The reddened edges 
become dusky in hue, and may be cracked and fissured also. The 
tongue is very slowly protruded on request, partly from mental 
apathy, partly from feebleness and because its surface is so stiffened 
that to move it is difficult. It is equally slowly withdrawn for similar 
reasons, and while protruded is often markedly tremulous. Toward 
the close of the attack the tongue cleans off through exfoliation of 
the dead epithelial accumulation, and this is a favorable or un- 
favorable sign according to whether the remaining surface is red and 
moist or dusky and dry. Sometimes these characteristic coatings do 
not appear, the tongue being brown and rough all through the disease. 
The heavily coated dry tongue just described is, however, rarely 
seen in those cases of intense fever which are treated by cold bath- 
ing. A small, triangular patch devoid of coating is often seen at 
the tip of the tongue in relapsing fever. 

In uremia the tongue is often dry, brown, cracked, and furred. 
The patient, if conscious, complains of a foul taste and the breath 
may smell like stale urine. 

In biliousness the tongue is coated almost uniformly by a whitish- 
yellow, pasty coat, extending from back to tip and side to side. The 
tongue is broad and flabby, and sometimes indented by the teeth, 
while the breath is foul and heavy. A similar tongue is seen in 
severe tonsillitis, except that it seems even more foul and less yellow 
in tint. Similarly in jaundice of the acute catarrhal type we have a 
coating still more yellow in some cases, because, as Fothergill 
asserts, the coat has been stained by the taurocholic acid eliminated 
by the salivary glands. The circumvallate papillae are often promi- 
nent and stand above the coating, which is easily removed on 
scraping. 

A broad, white, heavily-coated, moist tongue is often seen in acute 
articular rheumatism, becoming dry if the fever is high and the attack 
prolonged. 



THE TOXGUE 115 

The white tongue of a person who takes large amounts of milk is 
generally not smooth and pasty, hut rather rough in appearance. 
If the tongue be suffering from an attack of thrush (saccharomvce^ 
albicans), the white coating will consist of irregular white masses of 
the growth, which, if in great number, often coalesce and make a 
fairly even surface. The soreness of the mouth, the local heat, the 
salivation, and the age of the person — generally a young child — 
render the diagnosis easy. 

A grayish diphtheritic looking coating of the tongue, occurring 
in adults, may be due to the growth of various forms of mycoses. 
Thus, a fine network of leptothrix in threads and tufts often spreads 
over the tongue, particularly in the region of the circumvallate 
papillae. The growth may be quite dark in color, but it is sepa- 
rated from the exudate of diphtheria by microscopic study and the 
absence of systemic disturbance. 

Sometimes on examining the tongue of a child we find that it is 
broad and flabby and covered by a gray coating, which is smooth 
and fairly moist. Scattered throughout this coating are patches in 
which the coating and epithelium have been shed, leaving red spots 
with sharply defined edges, which spots are said to be "worm-eaten" 
in their appearance — that is, to have the irregular outline of the 
marks on a worm-eaten leaf. In these areas are to be seen enlarged 
and reddened fungiform papillae. Such a tongue is typical of what 
has been called, by Eustace Smith, "mucous disease" a condition 
in which there exists a more or less marked chronic catarrhal pro( « iss 
in all the mucous membranes. If, on the other hand, there is a 
comparatively light coating, dotted irregularly by bright-red spots, 
which are not raised above the surface, but are very numerous, and 
the patient is a child, the diagnosis may be made of acute or subacute 
gastric catarrh. 

The so-called "strawberry tongue" is one in which the organ is 
entirely denuded of coating and superficial epithelium, while the 
fungiform papillae are swollen or enlarged and stand our prominently. 
This appearance of the tongue is seen commonly in scarlet fever, 
but is not, as has been thought, pathognomonic of that disease. 
The fungiform papillae in the strawberry tongue of scarlet fever 
are, however, particularly prominent and erect. 

When the tongue is excessively furred or rough in appearance, 
the coating is due to abnormally long and projecting papillae covered 
by an excess of living and dead epithelial cells; it may denote grave 
disease of the viscera, but in rare instances possesses no diagnostic 
importance, unless coupled with other symptoms. This tongue is 
sometimes seen in scrofulous children in whom strumous manifesta- 
tions are marked. 

Should the tongue be denuded not only of coating, but, in addi- 



HO THE TONGUE, MOUTH, PHARYNX, AND ESOPHAGUS 

tion, of its normal epithelium, so that it appears dry, hard, and 
harsh to the touch, it denotes, as a rule, grave and advanced disease 
of an exhausting nature, such as renal, hepatic, or gastric disorder 
about to cause the death of the patient. Sometimes this condition 
is seen in advanced phthisis, diabetes, or gastric carcinoma, and is 
of evil omen. 

When the tongue is bereft of epithelium, beefy and red looking, 
elongated and narrowed, and shows a peculiar roundness when 
protruded, severe disease of the abdominal organs, such as 
dysentery, or hepatic abscess, or carcinoma, will often be found, 
or, in some cases, this condition develops to add to the discomfort 
of cases of advanced pulmonary tuberculosis or acute peritonitis. 
This tongue is sometimes called the " parrot tongue." 

In this connection the point should be noted that dryness of the 
tongue in the presence of grave disease is always an evil omen, and 
returning moisture of the tongue a favorable one. 

Unilateral coating of the tongue may be due to a decayed or ragged 
tooth, or to hemiplegia, which prevents that side of the tongue from 
being cleaned through movement. Hillow and Fairlie Clark both 
assert that morbid conditions of the second division of the trifacial 
nerve cause unilateral coating, and that abnormalities of the third 
division do not produce these changes as we would expect. 

The coating of the tongue is often so stained by extraneous sub- 
stances as to be entirely changed in appearance. If the coating be 
black, the color may be due to the ingestion of iron, of bismuth, 
charcoal, ink or blackberries, mulberries, cherries, or red wine. 
In very rare cases it is black, not from the growth of a fungus, 
as has been thought, but from overgrowth of the epithelium with 
the deposit of a black pigment of unknown origin. Usually this 
brownish-black discoloration is confined to the middle of the tongue. 
The affected surface is often rough, due to the enlarged papillae, 
and the edges of the spot are less black than the centre. In profes- 
sional tea tasters the tongue may be orange-tinted. 

The coating may be stained brown from the chewing of tobacco, 
from licorice, nuts, prunes, or chocolate, and yellow from the inges- 
tion of laudanum or rhubarb. 

The color of the tongue itself, aside from discoloration of its 
epithelium, is an important diagnostic aid. It is exceedingly pale 
in all forms of anemia, particularly those due to lack of hemoglobin, 
such as chlorosis or acute anemia from hemorrhage, and in per- 
nicious anemia, when well advanced, it has a remarkable pallor. 
It is livid and cyanotic in cases of pulmonary disease interfering 
with oxidation of the blood, or in cardiac disease with similar 
difficulty and when very large doses of coal-tar drugs have been 
taken, 



THE TONGUE 117 

Purple spots, which may be almost black, may be present on the 
tongue in Addison's disease. Sometimes they are bluish black, 
and always well defined and even with the surface. 

Very rarely the tongue is discolored by infarcts, blood stains, and 
bruises. 

When the tongue has its edges dotted with yellowish patches of a 
slightly elevated character, the condition is xanthelasma, and the 
liver will often be found to be disordered. 

In cases of poisoning by corrosive sublimate the tongue presents 
a most characteristic appearance, for it is white and shrivelled, and 
the papilla? at the base are unusually large. 

When sulphuric acid has been swallowed the tongue has a parch- 
ment-like appearance, is at first white and then gray or brownish 
gray, and finally is covered by a black slough, which as it separates 
leaves a swollen, excoriated patch. In nitric-acid and chromic-acid 
poisoning the tongue is shrivelled and lemon yellow in color, as it 
is when hydrochloric acid has been swallowed. The tongue of 
carbolic-acid poisoning is very characteristic indeed, for the mucous 
membrane is shrivelled and puckered into folds. The spots where 
the acid has touched it are brownish if impure acid has been swal- 
lowed, or white if the pure acid has been taken. In the course of 
a few hours this spot becomes surrounded by a red zone, and finally 
becomes dark brown or black in the centre. After oxalic add is 
taken the tongue may be covered by a thick white coat and looks 
as if it had been scalded. Caustic potash and soda soften the 
mucous membrane, so that it is pulpy and easily detached, and 
looks pearly, red, or yellow in hue. When ammonia is swallowed 
the color is white, but superficial edema may make it pearly in 
appearance, and acid nitrate of mercury renders it very red. Can- 
tharidal poisoning produces large lingual blisters and sores. 

Aside from the coating and color of the tongue, its surfaces should 
be examined to discover fissures, cracks, ulcers, sloughs, and swell- 
ings. The tongue is often seen to be superficially and irregularly 
fissured in old persons, particularly in those who have used large 
quantities of strong alcoholic drinks or strong tea, or who have 
chewed tobacco incessantly for many years. The fissures cross each 
other in every direction, although the central fissure which runs 
longitudinally is generally deepest and longest. If the furrows are 
very deep, they may indicate the early stages of what Wunderlich 
has called dissecting glossitis, which in turn may be due to syphilis, 1 
although, as a rule, the fissures of the tongue due to syphilis are 
deepest at the edges of the organ, and are due to pressure by and 
from irritation from the teeth or to ulceration, and subsequent 

1 This is denied by Demarquay and doubted by Butlin. 



118 THE TONGUE, MOUTH, PHARYNX, AND ESOPHAGUS 

cicatrization of small syphilitic nodules or gummata. The cervical 
glands are rarely involved in such cases. If only one ulcer is present 
it may be chancre, which will have the peculiar Hunterian hard base, 
and, in such a case, the cervical glands will probably be enlarged. 
An epithelioma may also have an indurated base with secondary 
glandular enlargement. Lingual ulcers may also be present as the 
mucous patches of syphilis, or be due to wounds from the teeth, a 
broken pipe-stem, or a fork. When these become chronic their 
separation from those due to syphilis and tuberculosis is practically 
impossible on superficial examination. Sometimes an ulcer of the 
tongue is due to epithelioma; but if this is the case, the patient will 
probably be past thirty years of age. As deep syphilitic ulcers 
heal sclerosis of the tongue may develop. 

Multiple ulceration of the tongue may be due to tuberculous dis- 
ease, which is very rarely primary, but rather secondary to its pres- 
ence elsewhere. The sores are often stellate in shape, and there 
is always swelling of the cervical lymphatics, whereas in multiple 
syphilitic ulceration of the tongue the glands generally escape. The 
diagnosis between tuberculous ulcer and that due to epithelioma is 
more difficult, since in both diseases the cervical glands are involved. 
Both are more common in men than in women. The age of the 
patient, the presence of tuberculous disease elsewhere, and the 
absence of induration point to tubercle. The tuberculous ulcer is 
not surrounded by much inflammation, is covered by grayish puru- 
lent mucus, and may contain bacilli of tubercle, and is often asso- 
ciated with tuberculous nodules which have not broken down. 

Ulcers of the tongue may also be due very rarely to lupus. A 
very similar tongue is seen in a tropical disease with intestinal 
disorder called by Thin "psilosis." An herpetic eruption appears 
on the tongue, which leaves large areas devoid of epithelium, while 
sinuous furrows or fissures develop. These fissures then heal, the 
patches become pallid, and recovery takes place. 

The various ulcerated surfaces so far described might be confused 
with ulcerative stomatitis, but their chronic character and insensi- 
tiveness as compared to acute ulcers of the tongue, associated with 
a specific history or manifestations of tuberculosis or syphilis else- 
where, render the diagnosis clear. 

An ulcer on the frenum may be due to whooping-cough, in which 
disease the edge of the lower incisors may injure the tongue in the 
paroxysm of cough, or, in adults, it may indicate the presence of a 
ragged tooth, which produces constant irritation, or, if the patient 
is advanced in years, represent the early stages of epithelioma, or 
that a broken pipe-stem has produced a wound. 

Very rarely the tongue partakes of the ulceration of the tonsils 
and roof of the mouth which is seen in cases of Schonlein's disease, 



THE TONGUE 119 

accompanied by purpuric eruptions on the skin and evidences of 
septicemia. 

Should the tongue be marked by bites from the teeth the 
patient may be an epileptic. Even if he denies that he is affected 
by the disease, the attacks may be unknown to him, because 
they are nocturnal. If the tongue is frequently bitten, the patient 
may be suffering from the early stages of glossolabiopharyngeal 
paralysis. 1 

The surface of the tongue may be attacked by various eruptions, 
such as measles, variola, eczema, herpes, erysipelas, pemphigus, 
zoster, or hydroa, and from the rupture of the vesicles or bullae so 
formed ulcers may arise. 

If the sore is herpetic, de Mussy asserts that the eruption will be 
found in the distribution of the lingual branch of the chorda tym- 
pani along the under border at the side. 

Sometimes the surface of the tongue is here and there devoid of 
epithelium, and in some of these patches excoriated. Pain may or 
may not be present. The condition is called chronic superficial 
glossitis by Hack, and is considered by some to be the same disease 
described by Kaposi as glossodynia exfoliativa. It is more common 
in men and lasts many years. 

Urticaria of the tongue has been reported by Laveran and xero- 
derma pigmentosum by Keating. 

The presence of a plaque on the anterior portion of the dorsum 
of the tongue to one side of the median line, which is raised, not 
ulcerated, but red and irritated looking, may be due to excessive 
smoking, the smoke irritating the local epithelium. It is always 
very smooth, later covered by a yellowish-brown coat, and is some- 
times called "smokers' patch." It may extend over the whole 
tongue and last for years. 

When the tongue has on its dorsum and edges dull-white or slate- 
colored dots, patches, or lines, which are elevated, hard, and horny 
to the touch, but not painful, the condition is known as leucokera- 
tosis buccal is, or leucoma or ichthyosis, and this may arise from 
smoking or glass blowing. It rarely begins in persons under twenty 
or in those over sixty years. It is often a strong predisposing agent 
toward cancer of the tongue. These spots are arranged on the 
tongue in longitudinal lines. Hyde asserts that they are due to 
excessive keratinization of the epithelium covered by an adherent 
and dense pellicle. The history is chronic, and ultimately by the 
stiffness of the spots the tongue may become cracked, and this in 
turn, perhaps, gives rise to carcinoma. 

When the tongue is covered by smooth, dense plaques and disks 

i It may be pointed out in passing that if there be fits, and biting of the tongue never 
occurs, and the patient is a female, the attacks are probably hysterical. 



120 THE TONGUE, MOUTH, PHARYNX, AND ESOPHAGUS 

or rings, the condition may be lichen planus, but the diagnosis of 
lichen planus from leucokeratosis buccalis is difficult, if not im- 
possible. The plaques are most commonly seen in males between 
twenty and forty years. Closely allied to this is the rare condition 
of hardening of the tongue due to scleroderma, as described by 
Kaposi. 

A very rare condition of the tongue is one in which its surface is 
marked by rings or areas on the dorsum, which gradually enlarge 
until they reach the edge or coalesce. In appearance they are red 
and smooth, deprived of filiform papillae, but not of the fungiform 
variety. Often the border of the circle is more red than the centre, 
and the very edge is often yellowish. This condition is sometimes 
called wandering rash, geographical tongue, or annulus migrans. 
Little if anything is known of its cause, save that delicate children 
are most often affected by it. 

Feeble, sickly children sometimes develop upon the tongue, as 
well as on the lips and cheeks, a condition in which a tenacious 
exudation is thrown out, the mucous membrane becoming fissured 
and sore. Gaston and Sebestre have called this stomatitis impeti- 
ginosa. 

Edema of the tongue, with the development upon it of vesicles, 
and, finally, sloughs, may occur, and is probably identical with the 
foot-and-mouth disease of domestic animals. 

Bilateral atrophy of the tongue is due to disease affecting the 
hypoglossal nerves in some part of their course in or below the 
nuclei. (See Paralysis of the Tongue.) It occurs as a symptom of 
glossolabiopharyngeal paralysis, in which case the tongue is shriv- 
elled and atrophied in patches, and in the later stages of the disease 
the organ has a crenated appearance. In other cases it is present 
in progressive muscular atrophy, and rarely in locomotor ataxia. 
It has also been seen in general paralysis of the insane. Unilateral 
atrophy may also occur from these causes, and Remak asserts that 
it sometimes arises from chronic lead poisoning. Any disease 
involving the hypoglossal nerves may so result. (See Paralysis of 
the Tongue.) 

Smooth atrophy of the base of the tongue when developed in a 
person under fifty years of age is a sign of syphilis. Virchow pointed 
out this fact, and it has been confirmed by others. 

In cases where the tongue is much enlarged the increase in size 
may be due to malignant growth, to macroglossia, which is a form 
of congenital lymphangioma, inflammatory hypertrophy, and syph- 
ilis, or acute inflammation from irritant poisons or foods. It may 
also be due to dermoid cysts, fibroma, lipoma, papilloma, angioma, 
myxoma, osteoma, and enchondroma. When it is due to acute 
glossitis the organ is seen to be several times its normal size, is pro- 



THE TONGUE 121 

truded from the mouth, and marked by the pressure of the teeth. 
The organ is also clumsy and stiff, and heavily coated on the back 
portion. There is a profuse flow of saliva, and swallowing and 
speech are almost impossible. Glossitis may also be due to mercu- 
rialism, to septic infection, and may be either unilateral or bilateral. 
The tongue may be greatly enlarged by actinomycosis. Great 
enlargement of the tongue may also arise in acromegaly and in 
myxedema. In the latter disease the organ is broad, flat, and 
soft. 

The Movements of the Tongue. — The movements of the tongue 
depend upon its innervation and its muscles, and afford valuable 
information in diagnosis. The rapidity of its protrusion in nervous 
and excitable persons when they are asked to show the tongue is 
noteworthy, and its constant rolling is often seen in persons who are 
feeble minded. In all diseases associated with mental hebetude its 
protrusion on request is very slow, although the patient will often 
do this act when all other orders to move parts of the body fail to 
produce a response. In the various forms of coma due to apoplexy, 
diabetes, uremia, and cerebral congestion this condition obtains, 
and it is very characteristic of typhoid fever. Often the tongue which 
has been partially protruded is left so, even when the patient is told 
to draw it in. When the patient finds it difficult or impossible to 
remove food from between the teeth and cheek by means of his 
tongue, and complains that the power of speech is interfered with, 
because the tongue is clumsy in its movements, he may be suffering 
from the disease known as glossolabiopharyngeal paralysis or pro- 
gressive bulbar paralysis. These lingual disorders are often the 
earliest signs of the disease. More rarely this disability of the tongue 
may arise from pseudobulbar paralysis, or what has been called 
glossolabiopharyngeal cerebral paralysis, a disease in which foci of 
softening occur in that portion of the cortico-muscular tract in which 
are the fibers which supply the muscles used in swallowing and 
speaking. This false type is separated from the true bulbar palsy 
by its sudden onset, an apoplectiform seizure, and other evidences 
of cortical disease. The tongue affords the most important points 
for differential diagnosis when a differential diagnosis is to be made 
under these circumstances, for in the false disease it does not waste 
or develop the reactions of degeneration, whereas in true bulbar 
paralysis these changes always speedily develop. 

Paralysis of the Tongue. — In apoplexy the tongue is protruded 
toward the paralyzed side, as it is also in the condition, already 
described, of hemiatrophy. The lesions of the hypoglossus which 
produce paralysis may be of cortical origin (unilateral), in which 
case the hemorrhage or other injury may be situated where the 
middle and inferior frontal convolutions form the anterior central 



122 THE TONGUE, MOUTH, PHARYNX, AND ESOPHAGUS 

convolution, 1 or in the supranuclear tract between the cortex and 
the medulla, or in the hypoglossal nucleus, or, again, in the infra- 
nuclear tract within the medulla. Insular sclerosis may very rap- 
idly cause lingual paralysis. Paralysis of the tongue may also 
result from injury to the hypoglossal fibers outside the medulla 
through meningitis or syphilitic or other growths. In still other 
cases pressure upon the nerve in its foramen may cause unilateral 
paralysis, or wounds of the neck, caries of the first cervical verte- 
brae, or cervical tumors may so result. Often in such a case the 
spinal accessory nerve is also involved. Very rarely, indeed, the 
tongue may be paralyzed by a hypoglossal neuritis. (Erb.) In rare 
instances hemiatrophy of the tongue is associated with hemiatrophy 
of the face without hypoglossal injury. (Gowers.) Girard asserts 
that the sensory part of the trifacial contains trophic filaments for 
the tongue, and that the unilateral wasting may be due to disease 
of this nerve. 

In paralysis of the facial nerve the tongue may be partially 
paralyzed through the fact that the lingualis muscle is supplied 
by means of the chorda tympani nerve. 

When a tongue which is paralyzed unilaterally is retained in 
the mouth, it is seen that its root on the paralyzed side is 
higher than the other, owing to the paralysis of the posterior 
fibers of the hypoglossus; but when it is protruded the 
tongue goes toward the paralyzed side because it is pushed out by 
the fibers of the genioglossus muscle on the well side. Finally, let 
us remember that if the tongue is paralyzed on one side the lesion is 
in the cortex or the pons on the opposite side of the body, or in the 
nucleus in the medulla on the same side of the body, or in the nerve 
after it has left the medulla. If it is bilateral paralysis the lesion 
is probably nuclear, because the nuclei are so closely situated that 
even a small lesion involves both of them, or it may be due to 
symmetrical disease of both sides of the cortex, the so-called 
pseudobulbar paralysis already spoken of. 

It should not be forgotten that paralysis of the tongue may occur 
as the result of diphtheria. 

Hirt asserts that the reaction of degeneration may be found 
in the tongue whether the lesion be cortical or in the nucleus. If 
the lesion is only cerebral, this reaction will probably appear very 
late. 

Tremor of the Tongue. — A tremor seen in the tongue may indicate 
a variety of nervous ailments or severe acute disease, as in typhoid 
and other severe infectious diseases, but the freedom from excessive 
coating and the absence of the ordinary signs of acute illness will 

i This is probably a fact, but not yet confirmed by autopsy, unless we consider Edinger's 
case of softening under this area, which affected the tongue only, as a typical one. 



THE TONSILS, SOFT PALATE, TEETH, AND PHARYNX 123 

separate the case of tongue tremor of acute disease from the tremor 
representing nervous ailments. 

An important point to be regarded in noting lingual tremor is 
whether the tremor or fibrillary movement is constant, or whether 
it appears only when the tongue is moved to and fro or protruded. 
In typhoid fever the tremor occurs on movement, whereas in glosso- 
labiopharyngeal paralysis when the mouth is open fibrillary move- 
ments of the organ are often marked, while the organ lies in the 
floor of the mouth powerless and beyond the control of the patient. 
Tremor of the tongue is also seen in a marked form in many cases 
of alcoholism, and associated with this tremor it will be noted that 
the protrusion of the organ is uncertain or in jerks. 

Spasm of the Tongue. — Spasm of the tongue may be unilateral or 
bilateral, most commonly the latter. It is seen very commonly in 
cases of chorea, particularly of the posthemiplegic type, and in 
hysteria. In the first disease the movements are characteristically 
choreic. In the latter the spasm may be tonic or clonic or alternately 
tetanic and irregular. 

Often the spasm in hysteria is unilateral. Sometimes it is clonic 
in puerperal melancholia. Spasm of the tongue is a common 
symptom in association with the twitching of the lips of general 
paralysis of the insane. Jerky movements of the tongue may also 
occur in insular sclerosis, but this is not the cause of the peculiar 
speech of that affection. 

Very rarely the condition of lingual spasm is due to irritation of 
the hypoglossus by some cause as yet unknown. The tongue is 
darted in or out or thrown from side to side and often injured by 
the teeth. The spasms, as a rule, are not constant, but come on 
in attacks which closely resemble epilepsy, in that they are pre- 
ceded by an aura. (Remak and Berger.) A very rare affection 
termed aphthongia (Fleury) is characterized by spasm of the tongue 
on attempting to speak. Romberg has recorded a case of lingual 
spasm due to irritation of the fifth nerve from lingual neuralgia. 

In that very rare condition called "Thomsen's disease, " "charac- 
terized by tonic spasms in the muscles during voluntary movements," 
the tongue may be involved, but in this case the other voluntary 
muscles will share in the affection 



THE TONSILS, SOFT PALATE, TEETH, AND PHARYNX. 

Having considered the diagnostic significance of changes in the 
appearance of the tongue in this chapter, and of the appearance of 
the lips in the chapter on the Face and Head, there is yet to be 
discussed the condition of the buccal mucous membrane, the tonsils, 



124 THE TONGUE, MOUTH, PHARYNX, AND ESOPHAGUS 

the soft palate, the teeth, the upper part of the pharynx, and the 
postnasal spaces. As almost all the conditions found in the latter 
regions are of interest to the rhinologist rather than the general 
practitioner, only one or two affections of these parts will be included 
in this work. 

The Teeth. — We can sometimes gain some information from the 
teeth as to the state of the patient. Normally the two lower central 
incisors are cut about the sixth to the eighth month, then the four 
upper incisors from the eighth to the tenth month, and the lower 
lateral and all the front molars from the twelfth to the fourteenth 
month. The canines are cut from the eighteenth to the twentieth 
month, and the posterior molars at two to two and one-half years. 
The first permanent teeth usually begin to come in about the sixth 
year. In children who are sufferers from rickets the teeth decay 
very early and rapidly, and if they be sufferers from inherited 
syphilis, the teeth are often cut in the early months of life. 

Caries of the teeth to an undue extent is also seen in many preg- 
nant women and in cases of diabetes mellitus. 

If the permanent upper incisors are notched or peg-shaped with 
notches in the free edge, as if cut out with a small gouge, they are 
a fairly sure indication of syphilis of an hereditary character (Hutchin- 
son teeth), and if in association with this deformity of the teeth 
we find middle-ear catarrh and keratitis, we have the " syphilitic 
triad," which is important as a sign of hereditary syphilis. These 
notches are not found in the so-called "milk teeth." 

The staining of teeth by tobacco or other materials held in the 
mouth may reveal certain habits of the patient, and a blue line on 
the gums where they join the teeth is an indication of the presence 
of chronic lead poisoning. Loosening of the teeth, with bleeding, 
spongy gums should call to the physician's mind the possibility of 
scurvy or scorbutus, and the spongy gums are particularly indica- 
tive of this affection in bottle-fed babies. If loosening of the teeth 
occurs in adults, it may be due to mercurial salivation. 

Grinding of the teeth in sleep in children usually indicates gastro- 
intestinal irritation from indigestion or worms, and it is sometimes 
seen in the advanced stages of respiratory diseases, as from pneu- 
monia or diphtheria associated with dyspnea. It takes place in 
adults in hysteria, maniacal attacks, and in epilepsy. 

The Buccal Mucous Membrane. — Swelling and redness of the 
buccal mucous membrane occur in the various mild forms of 
stomatitis, and in the ulcerative type of this disease the more severe 
lesions are often found in this area. In the malignant ulcerative 
stomatitis called noma the slough which separates from the inside 
of the cheek leaves a large excavation which may become so deep 
as finally to perforate the cheek. 



THE TONGUE, SOFT PALATE, TEETH, AND PHARYNX 125 

It is interesting to note that swelling of the check with great 
inflammation of the buccal mucous membrane is sometimes -ecu as 
the result of the formation of a salivary calculus in the duct of 

Steno, and it is also stated that obstruction from inflammation of 
this duct often occurs as a result of poisoning by sulphuric acid. 
This writer has seen a case of that rare malady called Schonlein's 

disease, in which, in addition to the multiple arthritis, purpuric 
eruption, and great edema, the formation of a large ulcer or slough 
threatened to perforate the cheek, and in healing produced a cicatrix 
which interfered with the patient's ability to open the mouth. This 
patient was an adult. 

The Tonsils. — If a patient presents himself to the physician with 
the statement that he is suffering from general pains all over t lie body, 
particularly in the small of the back, quite high fever it may be, with 
much sore throat and difficulty in swallowing, the trouble in the ma- 
jority of cases will be, in the adult, tonsillitis of the follicular form. 
If the symptoms are exceedingly seven 1 , the inflammation may result 
in suppuration — suppurative tonsillitis. It is to be remembered in 
all cases that the systemic or constitutional disturbance is out of all 
proportion to the severity of the local Lesions. If it is tonsillitis, 
the glands can be felt in the majority of cases a little beneath and 
forward of the angle of the jaw, and pressure upon them may pro- 
duce considerable pain. If the mouth is well opened and the tongue 
depressed, there will be found on each side of the throat a more or 
less projecting and inflamed mass, in the depressions or follicular 
openings of which will be found a white or yellowish exudate, which 
in severe cases may spread over the surface of the gland until it 
slightly resembles the membrane of diphtheria. Pressure on the 
tonsil may cause the further projection of these cheesy-looking 
masses. 

In the suppurative form of the disease the surface of the gland 
may be smooth and reddened, and in a day or two become soft and 
fluctuating, and if lanced pus will escape. 

The severe constitutional disturbance, the soreness of the throat, 
difficulty in swallowing, and the follicular exudate call to mind in 
all such cases the possibility of the disease being diphtheria; but in 
tonsillitis the exudate can be easily removed without leaving a 
bleeding surface behind it, and it has not the dusky, dirty look of 
diphtheritic membrane. Again, in tonsillitis the exudate is seen on 
the tonsils only, whereas in diphtheria it spreads over the half- 
arches and uvula. The general symptoms may make one suspect 
the onset of scarlet fever, particularly if the patient be a child; but 
the examination of the throat in scarlet fever shows the intense 
redness of pharyngeal mucous membrane with comparatively slight 
enlargement of the tonsils. The intense redness of the throat in 



126 THE TONGUE, MOUTH, PHARYNX, AND ESOPHAGUS 

scarlatina and the development of the rash on the skin aid in 
making a differential diagnosis. The lymphatic glands of the neck 
may be enlarged in scarlet fever, but are rarely so in tonsillitis. 

The Pharynx. — Difficulty in swallowing may arise from involve- 
ment of the pharyngeal muscles in diphtheritic paralysis, or from 
glossolabiopharyngeal paralysis. (See chapter on the Face, or Retro- 
esophageal Abscess.) Much more commonly it results from ton- 
sillitis or pharyngitis. Not rarely it is due to a stricture of the 
esophagus, and sometimes to a morbid growth in the walls of this 
tube, or to the pressure of such a growth situated in the surrounding 
tissues. If the difficulty in swallowing is due to diphtheritic par- 
alysis the history will be that there had recently been an attack of 
diphtheria. If due to a lesion of the bulb there will be the symp- 
toms described in the chapter on the Face, as referred to above. The 
presence of an inflammation of the pharynx or the tonsils is easily 
discovered by observation of the back part of the mouth, as is also 
retro-esophageal abscess, which will generally be found associated 
with disease of the cervical vertebrae. If these states be excluded the 
diagnosis now lies between a stricture and a growth, and as the 
growth may be an aneurysm the patient's chest should be carefully 
examined and the other signs of aneurysm sought for, for should 
this be overlooked and an esophageal sound passed, the aneurysm, 
if present, may be ruptured. This examination may also disclose 
the existence of a mediastinal growth or enlargement of the retro- 
esophageal glands. If these causes be eliminated the actual search 
for stricture may be begun. First the physician should listen over 
the cardiac orifice of the stomach while the patient takes a swallow 
of water. If the act of swallowing is properly performed this 
single swallow of water will be heard to descend to the cardiac 
orifice, and then pause there for six seconds before it falls into 
the stomach. If there is a stricture this fall will be delayed; if 
there be atony of the cardia it will be hastened. An ordinary esopha- 
geal bougie may be passed. If a point of resistance is discovered 
that part of the bougie stem opposite the upper incisor teeth is 
marked, and then the instrument is withdrawn. In this manner we 
are enabled to tell the part of the esophagus affected. Usually pain 
will be felt where the bougie is arrested; but care must be exercised 
that spasmodic contraction of the esophagus is not mistaken for 
stricture. In the former state gentle and persistent pressure will 
overcome the obstruction. Usually the stricture exists at a point 
about six inches from the teeth; or where the left bronchus crosses 
the gullet, about eight or nine inches from the teeth; or at the cardiac 
orifice, which is seventeen inches from the teeth in the adult. 

If a stricture exists it may be due to a cicatrix the result of 
an old burn, from the ingestion of alkalies or acids, or from an 



THE TONGUE, SOFT PALATE, TEETH, AND PHARYNX 127 

ulcer due to another cause. In other cases the lesion is due to 
syphilis. 

If the obstruction be due to cancer the passage of a bougie may do 
great damage, and, therefore, if any intimation of the existence of 
such a growth is present, great gentleness must be used. It should 
also be remembered that the bougie may be arrested by its passage 
into a diverticulum, or, in other cases, the instrument, by coiling on 
itself, may give a wrong impression as to the site of the obstruction. 
If a diverticulum is present the food which is obtained from it is 
usually alkaline, as it has never entered the stomach, and milk 
derived from a diverticulum, in which it has tarried a short time 
after attempted swallowing, will not be coagulated. 

In doubtful cases it is advisable to have the patient swallow a 
large dose of bismuth in mucilage of acacia and then examine the 
esophagus with the Rontgen rays. 

Finally, the physician should not forget, if his patient be a young 
woman, that there may be hysterical spasm of the esophagus. 

If the patient complains of dysphagia, and, on examination, the 
pharynx is red and the tonsils are covered with patches which speedily 
spread, as just described, so that by forty-eight or seventy-two 
hours the tonsils, pillars, and soft palate are covered by a gray mem- 
brane, the case should always be diagnosticated as diphtheria 
and treated as such, unless a bacteriological examination of the 
exudate shows the infection to be due to a streptococcus and not to 
the Klebs-Loeffler bacillus. Even if the patient has not true diph- 
theria, he may be exceedingly ill. Again, it is to be remembered that 
while some cases of scarlet fever which in their early stages present a 
membranous pharyngitis or tonsillitis are due to the streptococcus 
and not to the Loeffler bacillus, in the later stages of the disease the 
Loeffler bacillus is the cause of the local lesion. The differentiation 
is to be made chiefly by bacteriological tests, but it is worthy of note 
that the early formed streptococcic membrane does not spread 
as does the diphtheritic membrane, and does not return so rapidly 
when removed. The two diseases, diphtheria and scarlet fever, 
often exist simultaneously. Rarely the formation of a false mem- 
brane due to streptococcus infection, or still more rarely to the 
diphtheria bacillus, complicates the course of typhoid fever, and 
also occurs as a grave complication of measles. 

If in any case of diphtheria the false membrane extends to the 
nasal chambers, the prognosis is very unfavorable. 

Ordinary sore throat or acute pharyngitis is generally accompa- 
nied with little systemic disturbance, the local pain and soreness 
being the most characteristic symptoms. Inspection will show the 
pharyngeal wall red and angry looking, and very likely unduly dry. 

Care should always be taken, in the case of children particularly, 



128 THE TONGUE, MOUTH, PHARYNX, AND ESOPHAGUS 

that the early sore throat of measles and scarlet fever is not taken 
for simple pharyngitis. Often the rash of measles can be seen on 
the pharyngeal wall some hours before the rash appears on the skin. 
A peculiar eruption also develops on the buccal mucous membrane. 
This eruption consists of small, irregular red spots with a bluish- 
white centre, and should be looked for in a good light. Koplik 
believes that these spots are absolutely characteristic, and clinical 
experience endorses his view. (See Plate V.) Their absence, how- 
ever, does not exclude the presence of measles. They are to be 
distinguished from the reddened mucous membrane of scarlet fever, 
the large, white spots of thrush, and the sore mouth of stomatitis. 
They do not appear in rotheln. 

Pigmentation of the buccal mucous membrane often occurs in 
Addison's disease. 

Sometimes cases are seen in which there are tonsillar pain and 
irritation, and in which careful examination proves the discomfort 
to be due to the presence of a small calculus in a follicle of the 
tonsil. 

When swelling of the tonsils is chronic the enlargement of these 
bodies may produce mouth breathing, with the peculiar facies of 
that habit (see illustration in chapter on the Face), deficient thoracic 
and general systemic development, and a peculiar cough, constant 
in character and worse at night. Often the swollen or enlarged 
glands extending across the pharynx actually touch one another. 



PLATE V 



Fig. 1. 



Fig 2. 





Fig. 



Fig. 4. 





The Pathognomonic Sign of Measles (Koplik's Spots 



Fig. 1. — The discrete measles spots on the buccal or labial mucous membrane, showing the isolated 
rose-red spot, with the minute bluish-white centre, on the normally colored mucous membrane. 

Fig. 2. — Shows the partially diffuse eruption on the mucous membrane of the cheeks and lips; patches 
of pale pink interspersed among rose-red patches, the latter showing numerous pale bluish-white spots. 

Fig. 3. — The appearance of ,ne buccal or labial mucous membrane when the measles spots completely 
coalesce and give a diffuse redness, with the myriads of bluish-white specks. The exanthem on the skin 
is at this time generally fully developed. 



Fig. 4. — Aphthous stomatitis apt to be mistaken for measles spots. 
Minute yellow points are surrounded by a red area. Always discrete. 



Mucous membrane normal in hue. 



CHAPTER VI. 

THE SKIN. 

The color of the skin — Eruptions on the skin— Gangrene, ulcers, and sloughs 
— Scars, sweating, dryness, edema, hardness — Anesthesia and hemi- 
anesthesia — Paresthesia, hyperesthesia, itching. 

Mich information can be obtained by careful examination of the 
skin in many cases of disease. The examiner should make a note 
of the color of the integument, of its general nutrition, of its pliabil- 
ity, and of its sensibility. Naturally the eye at once takes in any 
eruption or scars which may mar its naturally smooth surface, and, 
as eruptions and scars are often the manifestations of more or less 
active systemic disorders, an insight into the presence of internal 
disease may be obtained from them. 



COLOR OF THE SKIN. 

The color of the skin in health in the white race depends 
upon the presence of pigment in the cells of the mucous layer of the 
epidermis, and in the corium in those parts of the body where pig- 
mentation is marked, or to the condition of the subcutaneous circu- 
lation or of the blood in the subcutaneous vessels. Thus we often 
find the skin of the perineum, scrotum, axillae, and of the lower 
abdomen much darker than elsewhere in persons in perfect health. 
Similarly we see a marked reddish or yellowish-brown hue in those 
parts of the skin which have been exposed to sun and weather, as a 
result of a deposition of pigment and an increased capillary cir- 
culation. With these normal alterations in color, however, we have 
little to do, for it is the abnormal colorations which interest us from 
a diagnostic standpoint. The most common of these changes in 
color due to pigment is jaundice; the next the chloasma of pregnancy 
or uterine disease, a condition usually limited to the face. Abdomi- 
nal growths due to tuberculosis, cancer or lymphoma, and tubercu- 
losis of the peritoneum also cause pigmentation of the skin, and in 
melanotic cancer there is often very dark discoloration, so marked 
as to be confused with that of Addison's disease. Again, it is not 
uncommon for persons who have hepatic torpor with constipation 
to develop what are called liver spots, in which the skin has rather 
9 



130 THE SKIN 

a dirty hue. Under the name of vagabond's "pigmentation" we« 
sometimes see discoloration induced by the irritation of the skin 
produced by lice and exposure to dirt and weather, and this is capable 
of being mistaken for the pigmentation of Addison's disease. Finally, 
we see the yellowish-brown hue of the skin due to tinea versicolor, 
the bronzing of the skin in Addison's disease, and the slate-blue 
hue of argyria or chronic silver poisoning. (See further on in this 
chapter.) 

The changes in color depending upon disturbance of the subcu- 
taneous circulation or on alterations in the blood are either local or 
general. In extreme nervousness flushing or blushing, due to a 
local vasomotor relaxation with increased blood supply, may redden 
the face and neck, or in hectic fever a hyperemia of the skin over 
the malar bones may give rise to an increase in color, which may 
be dusky red, due to imperfect oxidation of the blood. Consider- 
able cyanosis of the face and hands in a case of tuberculosis of the 
lungs is a very grave symptom. Again, we see in pneumonia a 
peculiar dusky red flushing of one cheek or of the entire face, and 
in erysipelas the zone of hyperemic redness is characterized by its 
sharp line of demarcation and its raised edge. In the alterations in 
color due to changes in the quality of the blood we have, as causes, 
anemia due to lack of corpuscles or of hemoglobin, arising from 
the various etiological factors producing such states. 

Jaundice. — Taking up the color changes due to pigment, we find 
that in jaundice the deposition of the biliary coloring matter varies 
in degree from a slight tinge or almost imperceptible yellowing to 
a dark citron or olive-green hue. 

In examining the skin for jaundice care should be taken not to 
do so by gas- or candle-light, for the yellow flame masks the biliary 
color. If the tinge is very slight, it may be made more marked by 
stretching the skin on the palm of the hand or by pressing upon the 
skin a glass slide so that the yellow hue shows through it. 

Having discovered that yellow coloring matter has been deposited 
in the rete mucosum, it remains for the physician to decide what the 
cause of the jaundice may be. In the first place, it must be remem- 
bered that jaundice may be hepatogenous — that is, arise from dis- 
order in the liver, or be hematogenous, from disorders of the blood 
with the setting free of blood pigment. The hepatogenous jaundice 
is by far the more common of the two conditions, and the most com- 
mon cause of this form of jaundice is catarrhal inflammation of the 
smaller bile ducts and the common bile duct which generally occurs 
in association with gastroduodenal catarrh. 

Hepatogenous Jaundice. — As a result of a catarrhal process the bile 
duct becomes blocked by the swollen mucous membrane and the 
mucus which is secreted ; the biliary coloring matter is absorbed into 



COLOR OF THE SKIN 13] 

the hepatic circulation and general circulation, and is by this means 
distributed over the body. Another common cause of hepatogenous 
jaundice is the obstruction offered to the flow of bile by the presence 
of a gallstone or gallstones in the ducts; and a third cause of obstruc- 
tive jaundice, so called, is pressure on the ducts by growths or inflam- 
matory products in the immediately adjacent organs, or of adherent 
inflammation in the ducts themselves, or by the presence of a round- 
worm in the duct. Very rarely the jaundice may arise from the 
pressure on the common duct produced by floating kidney. 

Jaundice very rarely arises from pressure on the ducts by an 
aneurysm of the abdominal aorta, or from aneurysm involving the 
hepatic artery. Three such cases are recorded by Frerichs. Jaun- 
dice has also been seen in aneurysms of the superior mesenteric 
artery as the result of pressure and in cases in which there has been, 
or is, perihepatitis, with displacement of the liver in such a way 
that the adhesions cause twisting or dragging on the ducts. 

Catarrhal jaundice of the acute type is generally produced by 
indiscretions in diet associated with exposure. The patient, after 
more or less marked symptoms of gastric and intestinal disturbance 
and indigestion, feels wretchedly. There is a premonitory mental 
heaviness, with languor and malaise, and within forty-eight hours 
or less the yellowing of the conjunctiva and skin appears. The 
temperature is generally subnormal to a slight degree. The tongue 
is heavily coated and often somewhat dry. There are marked In-- 
of appetite, great distress, headache, and depression of spirits. Ex- 
amination of the hypochondrium may reveal some local tenderness 
and slight hepatic enlargement, while the abdomen will be in some 
instances markedly tympanitic as a result of intestinal fermentative 
processes in the absence of antiseptic bile. The bowels are consti- 
pated, often refusing to move except with powerful purgatives. 
There is little pain, except headache. This condition lasts for a 
few days or a week, when the color of the skin and conjunctiva 
usually begins to fade and the normal hue is reached in the course 
of a week or more. 

The presence of persistent jaundice should raise the suspicion that 
it is due to more serious disorder than simple catarrhal inflammation. 

The jaundice from obstruction by stone may be due to blocking 
of the biliary duct, whereby there is a stagnation of the flow with 
reabsorption of the bile, or to stoppage of the flow by the presence 
of a stone in the common duct just as it enters the bowel. A differ- 
ential diagnosis as to whether the stone is in one or the other of these 
places is usually impossible. 

The jaundice of gallstone obstruction may be sudden or gradual 
in onset. If sudden, it is often, but not always, preceded by a 
violent attack of pain in the hypochondrium, or, in other words, 



132 THE SKIN 

hepatic colic, in which the agony is excruciating and is accompanied 
by nausea and vomiting. The area of the pain is, however, dis- 
tinctly hepatic, and it does not radiate down the inside of the thigh 
and into the testicle or penis as does that due to renal calculus. In 
place of the subnormal temperature so often seen in catarrhal jaun- 
dice, we find in obstructive jaundice that the temperature is often 
considerably raised, and this is particularly apt to be the case in 
those instances in which the onset is gradual and the jaundice per- 
sistent, being due to reflex irritation or septic absorption produced 
by the impacted stone, which may be scratching or ulcerating the 
lining membrane of the duct. The history of repeated attacks of 
gallstone colic, the presence of gallstones now and then in the stools, 
the discovery of gallstone crepitus on deep palpation, the age of the 
patient, who is generally in or past middle life, and the fact that the 
patient is a female, all point to gallstone as a cause of the jaundice. 
As a rule, there is great loss of flesh in all forms of jaundice. Should 
the jaundice be due to gallstones impacted in the ducts, and pro- 
ducing irritation or ulceration of their lining so that septic absorp- 
tion or " Charcot's fever" develops, the pulse may become more 
rapid and running, from the general feebleness which rapidly asserts 
itself. Rigors of extreme severity, followed by sweatings and 
marked febrile movement, develop in such cases, the chills occurring 
daily or periodically in a manner closely resembling those of inter- 
mittent fever. 

The jaundice of malignant disease pressing upon the gall ducts is 
usually not intense, and is characterized by the physical signs of a 
tumor, by the marked wasting of the patient, and, as a rule, by the 
very gradual onset of the pigmentation of the skin. Generally the 
lesion in such cases is carcinoma of the head of the pancreas. In 
jaundice resulting from cancer of the liver the growth must be so 
situated as to compress the ducts, consequently jaundice occurs in 
only about one-third of the cases. 

In connection with this possibility the law of Courvoisier is to be 
borne in mind. This law has been well expressed by Mayo Robson 
in the following words: " Jaundice with distended gall-bladder is 
presumptive evidence in favor of malignant disease, but jaundice 
without distended gall-bladder favors the diagnosis of cholelithiasis." 
While this law or rule is a good guide, it must not be forgotten, as 
pointed out by Kehr, that gallstones produce malignant disease. 
Thus Courvoisier found gallstones in 87.5 per cent, of malignant 
cases, Delano Ames in 95.4 per cent, of gall-bladder cancer, and 
Schroeder has reached similar conclusions. 

Jaundice is also seen in hepatic hypertrophic cirrhosis to a slight 
extent in a small proportion of cases, and it is to be remembered 
that in those cases of this disease in which delirium and muscular 



COLOR of Tin-: SKIS 133 

twitching occur the symptoms may resemble acute yellow atrophy 
of the liver, and that all forms of jaundice produce headache and 
may cause delirium. In acute yellow atrophy of the liver see below 
the liver is greatly reduced in size, whereas in hypertrophy it i> 
greatly increased in size; and in atrophy the temperature is subnor- 
mal, whereas in the jaundice due to hypertrophic cirrhosis it is apt 
to l>e above normal. Jaundice also may be a manifestation of acute 
poisoning by phosphorus, which condition is generally accompanied 
by hepatic swelling and tenderness and with coffee-ground vomiting. 

Jaundice is present in all fatal cases of yellow freer and often 
in cases which ultimately recover. It also is a constant symptom 
in Weil's disease, which is probably in reality a septic icterus, but 
it is very rarely seen in suppurative hepatitis. 

A fleeting and light hue of jaundice is sometimes seen in cases 
of chronic valvular cardiac disease in which compensation is grad- 
ually failing. Rarely this hue becomes deeper as the heart failure 
increases. This jaundice is due to engorgement of the liver (nut- 
meg liver), which in time results in catarrh of the bile ducts, with 
consequent obstruction to the flow of bile. 

In amyloid disease of the liver Bartholow states that jaundice 
occurs in about one-tenth of the cases as a result of enlargement of 
the lymphatics in the hilus with pressure on the hepatic duct. 
Similarly jaundice may result from the presence of echinococci, but 
this is not a common symptom of the growth of these parasites, and 
the disease is very rare in the United States. 

The association of gastric disorder with evidences of gastric dila- 
tation and jaundice should recall the fact that gastroptosis sometimes 
causes jaundice. 

Jaundice sometimes complicates diabetes. Under these circum- 
stances it may be regarded as a coincidence or a valuable diagnostic 
aid, for, as we have already stated, tumors of the pancreas by pressing 
on the common duct may cause jaundice, and. as is now well known, 
widespread disease of the pancreas may cause diabetes. Jaundice in 
a case of diabetes should, therefore, direct attention to the pancreas. 

In this connection it is well to remember that Hanot, under the 
name of diabete bronze, has described a pigmentation of the skin 
which contains iron (that of Addison's disease and melanemia does 
not), and which is associated with diabetes, hvpertrophic cirrhosis 
of the liver, and enlargement of the spleen. The coloration occurs 
most markedlv upon the face, limbs, and genital organs; the glyco- 
suria is abundant and slight ascites may be present, the lower limbs 
may be edematous, the loss of weight and strength is rapid, and 
death soon ensues from pneumonia or coma. Hanot and Marie 
both regard it as a disease distinct from ordinary diabetes mellitus. 
True diabete bronze is exceedingly rare. Up to 1897 only 30 



134 THE SKIN 

cases had been reported. In the 4 cases reported in America it 
is interesting to note that diabetes was not present. It is probably 
better to call the disease " hepatic cirrhosis with pigmentation." 

Other noteworthy symptoms of hepatogenous jaundice are intense 
itching of the skin; a very slow pulse when the patient is at rest, 
due to stimulation of the vagus by the bile in the blood; and stain- 
ing of the sweat due to the bile pigment may also be present.- 

When the gallstone produces active suppuration the fever be- 
comes more like remittent fever and the patient rapidly emaciates 
and presents all the signs of active suppuration. 

The urine in all cases of hepatogenous jaundice is heavily bile- 
stained (see Urine), and the stools are generally clay-colored owing 
to absence of bile in the feces. 

A very rare cause of jaundice is acute yellow atrophy of the liver, 
a disease which is seen somewhat more frequently in women than 
in men, and particularly in association with pregnancy. The age 
of occurrence is usually between the twentieth and thirtieth years. 
The symptoms begin with gastro-intestinal disorder, followed by 
headache, delirium, muscular twitching, and perhaps convulsions. 
Simultaneously with the onset of the headache the jaundice appears, 
the patient becomes typhoidal and dies from exhaustion, although 
recovery has been known to occur. The stools during the attack are 
clay-colored, and the urine contains leucin in disks and tyrosin in 
needle-like crystals. 

Hematogenous Jaundice is due, as its name implies, to breaking 
down of the blood to so great an extent that the liver cannot deal 
with the waste material with sufficient rapidity, and as a result 
altered hemoglobin is deposited in the tissues. Any poison which 
produces excessive hemolysis, such as picric acid and the coal-tar 
products, chlorate of potassium, glycerin, and poisonous mushrooms, 
may cause this condition to develop, and in extreme malarial disease 
(remittent and pernicious malarial fever), dengue, relapsing fever, 
pernicious anemia, pneumonia, and in other infectious maladies 
jaundice may be produced in this manner. It is particularly apt 
to occur in cases of marked sepsis. 

Jaundice sometimes occurs after severe hemorrhage of a prolonged 
character and in prolonged exhausting fevers, and is then due not 
to any local hepatic trouble, but to blood changes, with the produc- 
tion of urobilin in excessive amounts. The urine fails to carry off 
all the urobilin which is produced from hematoidin or bilirubin. 
This condition is called " urobilin icterus." 

In nearly all cases of hematogenous jaundice the discoloration of 
the skin is very slight, and the important fact is to be remembered 
that the stools are not light or clay-colored as in hepatic jaundice, 
but contain a normal or excessive amount of pigment. Again, the 



COLOR OF THE SKIN 135 

systemic symptoms of catarrhal or obstructive hepatic jaundice are 
practically absent in the hematogenous variety, and the jaundice is 
simply a minor symptom associated with more grave manifestations 
which characterize the individual infectious process. If the poison- 
ing is very marked, convulsions, coma, or active delirium may come 
on, but it is probable that these symptoms are due more to the poison 
of the disease than to the broken-down blood. 

Vierordt states that a very small amount of biliary coloring matter 
is often found in the urine of patients suffering from pyemic jaun- 
dice, and regards this as an important sign that the discoloration of 
the skin is due in a given case to blood changes and not to biliary 
obstruction, whereas an excessive amount of biliary matter in the 
urine indicates hepatic trouble. 

Jaundice sometimes complicates croupous pneumonia, and if 
hematogenous in origin is a most serious condition, for it usually 
indicates a fatal ending. When such an attack arises from catarrh 
of the gall ducts during an attack of pneumonia the condition is by 
no means so grave. 

There remains to be considered the jaundice seen in the newborn, 
usually within the first or second day of life (icterus neonatorum), 
which some believe to be due to a decrease in the blood pressure in 
the portal vessels subsequent to the arrest of the placental circula- 
tion, with consequent absorption of bile into the blood, owing to the 
comparatively high tension of this fluid in the bile capillaries. Others 
think this jaundice is due to breaking down of the blood corpuscles 
shortly after birth as the result of some mild infection. Probably 
both causes act in some cases. If the cause be altered blood pressure 
the prognosis is favorable, and recovery takes place in about ten days 
or two weeks; and if the cause be an infection, the condition often 
proves rapidly fatal. Should this jaundice of the newborn be very 
marked the patient may be suffering from congenital stenosis, or 
absence of the common or hepatic duct (which cause is rare) ; from 
septicemia, through infection by way of the umbilicus; from phlebitis 
of the umbilical vein, or from a hepatitis due to hereditary syphilis. 
In any of these latter causes death will probably occur, whereas in 
the mild form of icterus neonatorum the prognosis is very favorable, 
even though the discoloration lasts for weeks. The mild form of 
icterus neonatorum, if due to blood changes, is rarely accompanied 
by great discoloration of the urine, and the feces are usually no lighter 
than normal in color; but if hepatic disease be present, the urine is 
bile-stained and the feces are light in hue. 

Jaundice sometimes comes on in the course of acute ulcerative 
endocarditis, and has been mistaken for that of acute yellow atrophy 
of the liver, and it often appears as a symptom of pernicious malarial 
fever, with vomiting, diarrhea, and grave nervous symptoms. 



136 THE SKIN 

Rarely jaundice follows severe fright or extreme anger, and 
Da Costa states that it sometimes ensues after concussion of the 
brain. 

Other Changes in the Color of the Skin. — A condition of the skin 
characterized by yellow, more or less elevated patches, is xanthoma, 
which Murchison states often complicates hepatic disease, but in 
the writer's experience it is more commonly met with in gouty 
women or patients suffering from oxaluria. Its favorite distribution 
is about the eyelids, but it may appear elsewhere. Lesions similar to 
xanthoma sometimes appear in the course of diabetes (Hutchinson, 
Besnier), and under these circumstances generally develop suddenly, 
and spontaneously disappear after some weeks or months. 

When the skin of the entire body, the face being particularly 
affected, is of' a livid or bluish-slate color, resembling somewhat the 
appearance of a person exposed to rays of light passing through 
blue glass, the condition is that of argyria or chronic silver poisoning. 
This discoloration is so characteristic as to admit of no difficulty 
in diagnosis, since the absence of any circulatory or respiratory em- 
barrassment excludes the possibility of its being due to cyanosis. 
Owing to the small amount of silver now given internally by physi- 
cians, chronic argyria is becoming rare. The discoloration is due 
to a deposit of oxide of silver in the rete Malpighii. 

Discoloration of the skin of the entire body of a sallow, lemon- 
yellow tint, sometimes called a "muddy yellow" hue, is seen in 
persons who are sufferers from prolonged malarial poisoning, and in 
some cases the subjects of prolonged suppurative processes not tuber- 
culous in character. A greasy, yellowish skin does, however, occur 
as an accompaniment of some cases of pulmonary phthisis, and these 
cases have, as a rule, a gloomy prognosis. Often chronic hepatic 
disease, such as cirrhosis, produces this sallow appearance. 

A very rare but interesting condition of black discoloration of 
the skin, making it as dark as if gunpowder were rubbed into it, is 
met with in cases of ochronosis. Associated with this discoloration 
there is a similar darkening of the conjunctiva, which is particularly 
well marked at angles of the palpebral fissure and alkaptonuria, 
that curious state in which the urine reduces copper in Fehling's 
test. Autopsy reveals an intense darkening of the articular cartilages. 

Other changes in the color of the skin, which cannot be said to 
be due to deposition of pigment, although they seem to be caused 
by this, are seen most markedly in the peculiar yellowish, cheesy 
pallor of carcinoma, the greenish-yellow tinge of true chlorosis, the 
curious cadaveric hue of advanced pyemia, and the yellow skin with 
a greasy feeling in some cases of paretic dementia. 

Local pigmentation of the skin results from many causes, both 
local and systemic, direct and indirect. When brownish-yellow 



COLOR OF THE SKIN 137 

spots or streaks appear on the face, so that chloasma is developed, 
we should look for uterine or hepatic disturbance or pregnancy; 
they are practically large freckles of a more or less distinct brown 
hue. Sometimes on the skin of the trunk small yellowish-brown or 
chamois-skin colored spots appear accompanied by no other symp- 
toms except perhaps slight itching. This is due to phthiriasis versi- 
color or chromophytosis due to the growth of the parasite microsporon 
furfur. The diagnosis can be settled by painting the infected area 
with Lugol's iodine solution, when the spot becomes a dark-brown 
or mahogany color. This is called ''Allen's test." In other 
instances chloasmic spots or localized discoloration of the skin 
results from injury to the skin, as pressure by clothes, chafing, or 
after constant severe scratching in the course of eczema or pedicu- 
losis or scabies. If the pigment is found in the nuchal and sacral 
regions, it is probably from the scratching caused by pediculi; if on 
the body in irregular distribution, it may have been caused by 
prurigo. Again, the presence of a brown pigmentation of the skin 
in clearly outlined patches may indicate the earlier use of a fly blister, 
a mustard plaster, or other counterirritants, and a brown discolor- 
ation of the skin, which might possibly be confused with that of 
Addison's disease, is produced by the free use externally of oil 
of cade. Sometimes these spots are produced by the prolonged 
use of arsenic, and the writer has reported a case in which the 
coalescence of the spots produced a curious grayish-brown hue 
of the entire body, so that the man looked somewhat like a mulatto. 

Sometimes brown pigmentation of the skin of the neck and face 
appears as a symptom in exophthalmic goitre, and this disease may 
also produce similar lesions on the chest and wrists. 

Very closely resembling these spots is the bronzing of the skin 
in patches which is seen in persons suffering from Addison'* dis- 
ease: but although bronzing: of the skin is a somewhat constant 
symptom of Addison's disease, its presence is neither a positive nor 
negative sign in diagnosis, for bronzing is sometimes seen in cases 
in which the suprarenal capsules are normal. In some instances 
the bronze color deepens into a dark gray or even a black hue, and 
although the discoloration is generally in patches, it may extend 
over the entire surface of the skin, even to the edges of the finger 
nails. The nails, however, escape, as does also the mucous mem- 
brane of the lips, although the lining of the mouth itself may be 
dotted with pigmentation. The color is due to pigmentation of the 
rete Malpighii, and pressure has no effect on it. The symptoms of 
Addison's disease to be found associated with these skin changes are 
"anemia, general languor or debility, remarkable feebleness of the 
heart's action, and irritability of the stomach." (Addison.) 

The slate-colored skin of argyria or chronic silver poisoning can 



138 THE SKIN 

be readily distinguished from the bronze color of Addison's disease; 
but if a further test is needed, it will be found that washing the skin 
of argyria with a solution of iodine changes its color, while that of 
Addison's disease remains unaltered. 

White patches, or leucoderma, are also sometimes seen in cases of 
true goitre, and brown ones in tuberculosis. 

In carcinoma of one of the internal organs, or of the breast of 
an advanced stage, the appearance of the skin is drawn and unusu- 
ally smooth, often shiny or greasy looking, somewhat gummy and 
leathery to the touch, particularly where the integument is naturally 
dense. Although it is difficult to describe, this skin is almost path- 
ognomonic of carcinoma, although it may also be present to some 
extent in far-advanced cases of pernicious anemia or sarcoma. 

Pallor of the skin is due to absence of the normal pigment, to 
deficient blood, to central or local vasomotor disturbance as is typified 
by fainting, and far more rarely by Raynaud's disease. As a type 
of the pallor due to lack of pigment in the skin we see vitiligo, 
while the pallor due to pernicious anemia or pseudoleukemia and 
malaria is owing to lack of red corpuscles. Similarly, a pallor due 
to lack of hemoglobin is typified by chlorosis. (See chapter on 
the Blood.) In all of these diseases the skin may be of ghastly 
whiteness or tinged with yellow. The skin is apt also to be very 
white, and even chalky in appearance, in chronic contracted kidney 
and chronic parenchymatous nephritis. 

In chlorosis the entire surface of the body is exceedingly pale, 
and the skin of the face, particularly about the mouth and nose and 
eyes, is somewhat greenish in hue. The skin of the cheeks may, 
however, be flushed and the lips abnormally red in hue. 

A very important diagnostic point to be remembered is that red 
cheeks often cause the physician to overlook well-advanced anemia 
in young women. (See chapter on the Blood.) 

In those cases in which the skin is pale from alteration of the 
subcutaneous circulation there is usually incompetence of the heart 
or vasomotor disturbance, but the most marked form of general 
pallor is that due to myxedema. 

Cyanosis, or blueness of the skin, depends upon the circulation in 
the subcutaneous vessels of imperfectly oxidized blood. The small 
veins are often seen to be swollen, particularly those of the face and 
the hands and feet. The most marked form of cyanosis with which 
we meet is the cyanosis of the newborn child, suffering from a patu- 
lous foramen ovale, and in this condition the color may vary from a 
slate hue to an almost black hue. The lobes of the ears, the tongue, 
the scrotum, and the toes show the color most deeply. It is impor- 
tant to remember that this form of cyanosis is greatly decreased, as 
a rule, by placing the child on its right side. Anything which pro- 



ERUPTIONS ON THE SKIN 139 

duces excitement increases the cyanosis greatly, whereas cyanosis 
due (o other causes is not subject to great variations. In the cya- 
nosis of the newly born, males are far more frequently affected than 
females, in the proportion of about 2 to 1 or 3 to 1, and it is a note- 
worthy fact that even when the cyanosis is due to a malformation 
of the heart it may not be present from the time of birth, but may 
develop several days afterward. J. Lewis Smith records II cases 
in which the cyanosis due to congenital heart lesion came on at 
periods ranging from two weeks to forty years after birth. 

About 35 per cent, of the cases of cyanosis due to congenital detects 
die in the first year. 

In cyanosis of the newborn the chances are about 10 to 1 that 
the lesion is absence of a properly developed interauricular or 
interventricular wall. 

In the adult or child cyanosis may be produced by serious cardiac 
disease, by pulmonary disease 4 , such as pneumonia, pulmonary con- 
gestion, and bronchiectasis with emphysema and associated cardiac 
dilatation. It also occurs in laryngeal obstruction arising from 
external pressure or intralaryngeal difficulty, and in cases of asthma 
of a severe form. (See chapter on the Thorax and its Viscera.) 

In some cases of paretic dementia the skin of the forehead is dull 
and dusky-looking. In other instances a grayish-blue or cyanotic 
appearance may arise from the ingestion of drugs which reduce the 
hemoglobin of the blood, such as antipyrine or acetanilid, and in 
such instances the discoloration is first seen about the base of the 
thumb nail or in the skin of the face, particularly if the patient be 
examined from a little distance. 

The condition of the skin, so far as its nutrition is concerned, is 
of great importance in diagnosis. In profound failure of the vital 
forces continuing over a great length of time it becomes abnormally 
dry and scaly, the hair becomes straggling and lustreless, and fre- 
quently falls. In young persons suffering from grave disease of the 4 
lungs or heart of a chronic type there is often not only an undue 
dryness of the cuticle, but an abnormal growth of downy hair all 
over the body and limbs, and more particularly down the spine and 
over the breast bone. 



ERUPTIONS ON THE SKIN. 

The influence of age upon the development of skin lesions is 
very great, and Stephen Mackenzie has summed up the relation- 
ship of skin diseases to age in the following amusing manner: 
"The seven stages of man could be well illustrated by disease of the 
skin, though we lack a Shakespeare to do justice to the theme. In 



140 THE SKIN 

the 'mewling and puking' infant we meet with sclerema and edema 
neonatorum, the 'red gum' or strophulus of the older writers, inter- 
trigo, eczema, urticaria papillosa (lichen urticatus), urticaria pig- 
mentosa, xeroderma pigmentosum, and impetigo; the 'school boy,' 
with his chilblains and ring-worms, alopecia areata, pityriasis rosea, 
ecthyma, and 'foot-ball disease;' and then the 'lover,' with his acne 
and sycosis, and, as a result of irregular sexual excursions, his 
syphilides; 'and then the justice, in fair round belly/ with acne 
rosacea, diabetic boils, and pruritus ani; the sixth stage shifts into 
the 'lean and slippered pantaloon,' with rodent ulcer and 'gouty' 
eczema; 'last scene of all, sans teeth, sans eyes, sans taste, sans every- 
thing' — except an incessant and intolerable itching of the skin 
which we call senile prurigo." 

There are two conditions of the skin in which valuable evidence 
is given that the patient is suffering from rheumatism. One is the 
presence of erythema in one of its many forms, the other is the ap- 
pearance of purpura, or, as it has been called, peliosis rheumatica. 
That the presence of erythema is often associated with lithemic or 
true rheumatic infection is proved beyond all doubt, either erythema 
papulatum, annulaire, marginatum, or nodosum being indicative 
of the systemic state, but it is worthy of note that the erythema 
marginatum is most diagnostic and erythema nodosum the least 
diagnostic of rheumatic poisoning. Sometimes this eruption may be 
the only manifestation of the disease other than cardiac involvement, 
and when it is marginate severe cardiac lesions are commonly pres- 
ent. The papulate eruption is most commonly found on the back 
of the wrists, the hands, and the feet when it occurs as a rheumatic 
sign, while the nodose variety is generally confined to the front aspect 
of the legs or the extensor surfaces of the arms. It is to be remem- 
bered that these forms of erythema may be distributed anywhere 
over the body in rheumatism, but that they become especially diag- 
nostic if limited to the areas named. 

Purpuric Discolorations of the skin, somewhat resembling minute 
multiple bruises in appearance, are due to a number of causes and 
possess a varied significance. In the first place, they are due to the 
condition known as purpura hemorrhagica, which may be divided 
into the acute and subacute forms and that which is secondary as 
the result of severe infections and certain poisonings. The acute 
form of purpura is probably in all cases a manifestation of an in- 
fection by a pathogenic organism runs a rapid course and reaches a 
fatal result in most cases in a short time. It is a comparatively 
rare disease and usually attacks young adults, chiefly males, up to 
twenty-eight years of age. It is sometimes seen in young girls and 
more rarely in young pregnant women. The chief symptoms con- 
sist in hemorrhages from the mucous membrane, purpuric spots 



ERUPTIONS ON THE SKIN 141 

high fever, and a general class of symptoms resembling those of 
sepsis, as chills, pyrexia, and exhaustion. In other instances active 
hemorrhages take place into the viscera, and if into the meninges of 
the brain cause cerebral symptoms at once. The liver and spleen 
are nearly always enlarged. 

The subacute type of purpura, while severe, runs a far more favor- 
able course as to its manifestations and results. It usually attacks 
children or young adult males from twenty to thirty years of age. 
The patient, after a feeling of wretchedness, and perhaps a chill, 
followed by the purpuric eruption, is attacked by swelling of the 
joints and perhaps hemorrhages from the kidneys, bowels, and 
mucous membranes. If the hemorrhage is from the gums, the teeth 
are not loosened, as in scurvy. Prostration may be great and the 
patient may appear as if suffering from typhoid fever. The prog- 
nosis is good for ultimate recovery. It is sometimes called peliosis 
rheumatica or Schonlein's disease. This subacute form, however, 
sometimes occurs in a more severe manner, as "Henoch's disease," 
in children between nine and twelve years, and is much more 
common in males than females (5 to 1). In this form we have 
as additional symptoms marked pain and tenderness in the belly, 
and bloody stools, with tenesmus and active vomiting. The illness 
may last a long time, but recovery often occurs, about 25 per cent, 
dying. 

The joint symptoms of the mild forms of purpura may be slight 
or absent. Often, too, the purpura is accompanied or replaced by 
erythema. 

The question as to whether purpuric eruptions are ever truly 
indicative of rheumatism has been much discussed. When purpura 
develops in the course of true articular rheumatism it is often an 
indication of an associated infection. In many cases, however, the 
arthritic inflammation is not a true rheumatism but in reality a 
septic arthritis which is due to the same cause as the purpura. In 
either case the eruption appears as a rule in the neighborhood of 
the involved joints, nearly always on the lower limbs, often breaking 
out before any evidence of articular trouble exists. In other in- 
stances the development of the purpura is simultaneous with the 
disappearance of joint trouble. The eruption usually fades in a few 
days, but frequent relapses or new crops of it often occur. 

Purpuric eruptions may be produced by quinine in persons who 
have an idiosyncrasy to this drug, and by iodide of potassium, 
chloral, and salicylic acid. They may also accompany any severe 
infectious disease and follow the entrance into the body of any poison 
which destroys the blood, such as the poison of snake bite. They 
also result from severe jaundice, from profound anemia, from con- 
genital syphilis with vascular changes, in ulcerative endocarditis (a 



142 THE SKIN 

form of sepsis), and in cases of multiple sarcomata. Rarely purpura 
has followed fright and severe grief. 

Hemorrhages into the Skin occur spontaneously in some cases of 
hysteria and paretic dementia, and after epileptic attacks, particu- 
larly about the eyes, and often from injuries received in other parts 
of the body during the convulsion. Minute hemorrhages may also 
occur in the course of severe whooping-cough, and, in the form of 
petechia?, result from snake poisoning, septicemia, cerebrospinal 
meningitis, iodism, ergotism, and after inhaling the vapor of benzine. 
They are also seen in scurvy and in some cases of profound wasting, 
as in the course of phthisis and carcinoma. 

Petechial rashes closely resembling those of malignant smallpox, 
typhoid fever, or cerebrospinal fever may be due to the presence 
of acute ulcerative endocarditis. 

Hemorrhages sometimes appear in the skin covering a part which 
has been affected by a severe pain in a crisis of locomotor ataxia. 

A very extraordinary manifestation of spontaneous subcutaneous 
hemorrhage is seen in what is known as hematoma auris, a condi- 
tion in which a free extravasation of blood takes place into and 
beneath the skin of the ear. The color of the swollen ear is quite 
red, if the hemorrhage has been recent, or dark blue if it is an old 
occurrence. The left ear is more commonly affected than the right, 
and it is seen more commonly in males than in females. 

The development of polymorphic skin lesions, consisting of hyper- 
emia, edema, and hemorrhage, with arthritis occasionally and vis- 
ceral disturbances, consisting in attacks of vomiting or diarrhea, 
endocarditis, pericarditis, acute nephritis, and hemorrhages from the 
mucous membranes, indicates the presence of a condition called 
erythema exudativum multiforme. The attacks are apt to be recur- 
rent. Sometimes the skin manifestations are absent. 

Subcutaneous Fibroid Nodules sometimes occur in cases of rheu- 
matism and vary in size from a hemp-seed to a walnut. They are 
usually situated in the subcutaneous connective tissue, but may be 
attached to the deep fascia or muscular sheaths. 

Intense redness of the skin is seen in acute inflammations of the 
skin or the subcutaneous tissues, and as the result of hot appli- 
cations, the redness being marked in proportion to the degree of 
heat and the time it is applied. Often the prolonged use of high 
heat will produce a peculiar mottling of the skin like that of an old 
bruise. 

Aside from the redness of the cheeks and forehead from blushing, 
we should remember the general flushing seen so commonly in 
persons suffering from phthisis, particularly when they are excited, 
which differs from the more dusky redness seen over the malar 
bones in hectic fever. 



ERUPTIONS ON THE SKIN 1 \:>, 

Urticaria may occur as a manifestation of rheumatism, but it lias 
110 diagnostic value. Sometimes it ensues upon the use of salicylic 
acid or turpentine, and quite commonly follows the ingestion of 
iodide of potassium. The wheals produced by the latter drug differ 
from those of urticaria in being unduly red. 

Very closely allied in its causes and appearance with urticaria of 
the severe type is angioneurotic edema. In this condition there 
appear upon the skin numerous patches or plaques of circumscribed 
puffy swellings, which have a red appearance and vary from the 
size of a nickel to a silver dollar or larger. There is an absence of 
itching, an important difference from true urticaria, but the part 
affected may be tense or hot to the patient. These attacks arc 
generally recurrent, and take place in neurotic persons. They may 
cause loss of sight through swelling of the eyelids, and, where the 
mucous membranes of the pharynx and larynx are involved, serious 
interference with breathing. The swelling of angioneurotic edema 
does not pit, and it is to be separated from the blue edema and 
white edema of hysteria. True angioneurotic edema is rare in 
hysteria, and if localized swellings do result from this condition the 
physician will generally find marked hysterical signs manifested, 
such as disorders of sensation or tenderness over the ovaries. 

Myxedema. — When the skin is pale and affected by an edematoid 
swelling, with loss of elasticity, particularly about the face, and 
also in the trunk and extremities, and if this swelling, which 
resembles edema, fails to pit on pressure, the physician should re- 
member that myxedema or the cretinoid edema of Gull may be 
present. If in addition to these signs there is a half-idiotic or 
heavy expression of the face, a slow and labored manner of speech, 
with thickened, clumsy fingers, the diagnosis is made practically 
certain. The brain in this disease perceives or grasps ideas very 
slowly, and all the functions of the body seem torpid. 

There are several other diseases in which great thickening of the 
skin takes place, which cannot, however, be confounded with myx- 
edema. In elephantiasis there is an hypertrophy of skin and sub- 
cutaneous tissues which is confined to some particular region of the 
body and arises from local circulatory disturbance in the blood and 
lymph vessels. The skin is very hard, so that the leg, if affected, 
feels like a solid mass of wood. The disease most commonly affects 
one of the legs, rarely both, and the scrotum. In both myxedema 
and elephantiasis the process develops very slowdy. 

Scleroderma. — When the skin is dotted with irregular patches or 
streaks, which may be elevated or tightly stretched, or if the entire 
skin is thickened, covered with thin scales, or possesses a plaster- 
like appearance, the physician should recognize these symptoms 
as indicative of scleroderma. If in addition to these signs there is 



144 THE SKIN 

a fleeting pitting of the skin on pressure, and it cannot be pinched 
into a fold, the diagnosis is confirmed. Sometimes the skin is sclero- 
dermatous, seems bound down by tense cords or bands of retracted 
connective tissue to the tissues beneath, and in rare instances even 
the tendons, muscles, facise, and joints may be involved. Generally 
the impaired movements of the joint depend upon the stiffening of 
the skin, but in some cases the disease results in atrophy of these 
deeper parts. 

If during the first months of life the skin of an infant becomes 
edematous, hard, tense, and glossy, varying in color from a white 
to a reddish or dirty yellowish brown, and if this rapidly involves 
the entire surface so that the integument becomes cool, immovable, 
and resistant, the child appearing as if frozen into stiffness, it is 
probably suffering from sclerema neonatorum, a disease entirely dif- 
ferent from the scleroderma of the adult. As a rule, death speedily 
ensues, but before this takes place the parts first affected become 
thin and lose their swelling and may develop cyanosis and gangrene. 

The affection just described is to be separated from edema neona- 
torum, a condition arising in prematurely born children. Within 
a few days after birth there is discovered a pallid, cold condition of 
the buttocks, thighs, legs, and arms. The parts speedily become 
edematous and livid blue. Finally, the edema may become very 
marked and the skin tense in consequence. Intense drowsiness is a 
characteristic of the disease. Death commonly ensues, but recovery 
may occur. While the color of the skin may be identical in edema 
neonatorum and sclerema neonatorum, the former affection lacks 
the stiffness of the jaw and other joints, and the pitting on pressure 
is marked. As scleroderma does not occur before the first year, it 
can be excluded from the diagnosis. 

Another interesting diagnostic sign in the skin is what is known 
as the "tache cerehrale^ a condition of vasomotor disorder in which 
when the finger is gently drawn over the skin of the forehead a red 
patch speedily develops. It is seen in meningeal irritation, brain 
abscess, epilepsy," in some cases of exophthalmic goitre, and in 
paretic dementia. Sometimes it is called "tache merdngeale" 

Erythema or Rose Rash, sometimes called roseola, is a redness of 
the skin, and occurs in many pathological conditions. It may be 
localized or diffused. In a number of diseases it aids very greatly in 
reaching a diagnosis, but the physician should always be cautious 
in depending much upon it, since it may mislead, owing to the fact 
that it often appears when devoid of diagnostic importance in so 
far as the eruptive fevers are concerned. (See page 147.) 

The Rash of the Acute Infectious Diseases.— The development 
of a diffuse, punctated rose rash on the skin of a person who is suffer- 
ing from malaise, fever, nervous disturbance, and sore throat should 



ERUPTIONS ON THE SKIN 145 

direct the physician's attention to the possible presence of two infec- 
tious diseases, namely, scarlet fever, which is more common in 
childhood, and syphilis, which is more frequent in adults. 

Scarlet Fever. — The rash of scarlet fever is usually of a bright-red 
color, and shows itself at the end of the first or on the second day of the 
disease, first appears on the chest, and neck, and then speedily involves 
nearly the whole surface of the body, although the forehead often 
escapes and the skin about the corners of the mouth remains nearly 
always white and free from eruption. On the other hand, the soles 
of the feet and palms of the hands are very markedly affected. So in- 
tensely reddened is the patient's surface that it may have the color of 
a boiled lobster. This redness depends upon an acute hyperemia 
of the skin, which though removed by pressure instantly returns 
when the finger is withdrawn. A noteworthy point is its punctate 
and mottled appearance, for, while the entire skin may be red, there 
are points which are more red than the rest of the skin, and also 
certain areas which arc particularly so. The skin is often slightly 
swollen and feels tense, and itching is commonly present. The rash 
usually lasts three or four days, and then fades, desquamation of the 
cuticle speedily setting in, which is complete in about two weeks. 
Sometimes, however, it remains for ten days to three weeks. Often 
w r hen the rash can scarcely be seen on the skin its full development 
will be found on the pharyngeal wall. In the malignant types of 
scarlet fever petechia? and subdermal hemorrhages occur. Some- 
times in scarlet fever fine miliary vesicles develop chiefly in the 
neighborhood of the axilla 1 or on the abdominal wall or thorax 
anteriorly. 

Sometimes, too, in those cases of scarlet fever which have severe 
symptoms of ulcerating sore throat with ear or nose complications 
there develops, about the third week of the disease, a dark-red 
papular or macular erythema on the extensor aspects of the large 
joints. It is a grave symptom. 

Rotheln. — The rash of rubella or rubeola or rotheln (German 
measles) more closely resembles that of scarlet fever in some 
cases than it does that of measles, but it is never as scarlet, is dis- 
tinctly maculated, and only at a distance looks homogeneous. Like 
measles, it is first seen on the face, chiefly about the nose and on the 
upper lip. Close examination always reveals the rash in oval 
patches or crescents, and it lacks the diffused character of the rash, 
the punctation of the skin, the grave systemic disturbance, and the 
throat symptoms of scarlet fever. Further, the febrile movement 
is comparatively slight, and the rash lasts only twelve hours or at 
the most for two or three days. Slight desquamation may, however, 
occur. 

Rotheln, or German measles, is separated from true measles in 
10 



146 THE SKIN 

many cases by the marked glandular enlargements, chiefly the pos- 
terior cervical, axillary, and inguinal; but this is also constantly 
true of scarlet fever and sometimes of measles. It never presents 
"Koplik's spots" on the buccal mucous membrane. (See chapter 
on the Tongue.) 

Measles. — The eruption of measles is very characteristic, and can 
be in most cases easily separated from the other exanthemata by 
close examination. It is a roseola in character, but more dusky 
than that of scarlet fever. It appears about the fourth day of the 
illness in association with catarrh of the mucous membrane of the 
eyes and .respiratory tract. Unlike scarlet fever it appears in 
macules first upon the forehead or face, then on the neck, trunk, 
and limbs. The macules, which often coalesce, are arranged in 
crescents which are red, but become somewhat yellowish on press- 
ure. They are slightly raised. There is nearly always to be seen 
some uninvolved skin, the entire surface not being covered as in 
scarlet fever. In some instances in which the eruption is aberrant 
a diagnosis of measles from scarlet fever is admittedly impossible 
until the case has been watched for some days; but the slow onset 
of measles, in which the eruption appears on the fourth day as 
against the first day in scarlet fever, the swollen eyes and nose, the 
puffiness of the face, the catarrhal condition of the mucous mem- 
branes, the curious fall of temperature after the preliminary rise on 
the first day, the short duration of the rash, all aid in the diagnosis 
of measles. The dusky eruption of measles can nearly always be 
found on the pharyngeal mucous membrane. (For the mouth and 
throat symptoms of scarlet fever and measles, see chapter on the 
Mouth and Tongue.) 

An erythema or roseola sometimes appears on the skin of chil- 
dren after vaccination, generally about eight to ten days after the 
operation. It rarely lasts more than two days, and on its disap- 
pearance there is slight desquamation. 

It also appears sometimes in cases of smallpox previous to the 
outbreak of the true eruption. Under the latter circumstance it is 
found most commonly about the groin and inner surface of the 
thighs and on the hypogastrium, loins, clavicles, and the extensor 
surfaces. So closely may the early rash of smallpox simulate the 
aberrant type of measles as to lead to grave mistakes in diagnosis. 
Sometimes an immediate diagnosis is impossible, even by the most 
experienced, but the rash of measles commonly appears on the face, 
therefore this difference, coupled with a history of exposure, the 
gradual development of the peculiar "shot under the skin" sensa- 
tion of variola, and the ultimate distinct papulation, vesiculation, 
and pustulation of smallpox soon remove the doubt from the 
physician's mind. 



ERUPTIONS o.V THE SKIN 147 

Day of Eruption of the Various Exanthemata. 



Day. 


Disease. 


Area 


First to second da^- .... 


Rotheln or German measles. 


Face first. 




Varicella or chickenpox. 


Face or trunk. 


Second day 


Scarlet fever. 


Neck and chest 


Third to fourth day .... 


Measles or morbilli or rubeola. 


Face. 




Variola or smallpox. 


Forehead, face, and wri-ts. 


Fourth to fifth day 


Typhus or ship fever. 


Trunk. 


Seventh to ninth day .... 


Typhoid or enteric fever. 


Abdomen. 



The remembrance that the incubation period of variola is twelve 
days, that of varicella seventeen days, of measles ten days, of rubella 
twenty-one days and of scarlet fever two to four days, will aid the 
diagnosis if a history of exposure can be obtained. 

A diagnosis between the eruption of measles and variola often 
can be made by stretching the skin between the fingers, when, if it 
be measles, the papule cannot be felt, whereas, if it be variola, it 
persists. This is called the "grisolle sign." 

An erythema resembling scarlet fever, not only in its appearance, 
but also by its association with swelling of the lymphatic glands 
and reddening of the mucous membranes of the mouth, sometimes 
develops about the second or third day in eases of dengue or break- 
bone fever. 

In children there are several other conditions than scarlet fever 
which are associated with rose rash, and these are prone to lead 
to grave errors of diagnosis not only because they may be mis- 
taken for scarlet fever but chiefly because a mild attack of scarlet 
fever may be considered as of their nature. The most frequent of 
these is erythema roseola, or roseola of acute indigestion, or that 
following the use of a food to which the patient has an idiosyncrasy. 
It is generally, but not always, widely diffused and is often associated 
with acute and severe febrile movement and vomiting, but it can be 
separated from scarlet fever by the facts that there is an absence 
of severe constitutional and nervous symptoms (except in neurotic 
children), there is no sore throat or enlarged cervical glands, and the 
rash does not come out on the clavicles and gradually travel down the 
body. Roseolous eruptions also appear in persons with delicate 
skins after coming in contact with irritant plants, and Dukes asserts 
that they may develop from handling caterpillars. 

The severe cases of scarlatina are easy of diagnosis. It is those 
in which the rash and sore throat are mild that are difficult of deter- 
mination. In these cases the physician must delay his diagnosis 
until the subsequent course of the malady enables him to marshal 



148 THE SKIN 

before his mind's eye most of the characteristic manifestation of true 
scarlet fever. 

Another condition closely resembling scarlet fever is rarely seen, 
namely, acute exfoliating dermatitis, called, in its mild form, ery- 
thema scarlatiniform, which has a sudden onset with febrile move- 
ment and a rash which rapidly spreads over the entire body and lasts 
four or five days, finally ending in desquamation So closely may 
this disease resemble scarlet fever that a diagnosis during the first 
attack may be impossible for the first few days, but the condition of 
the throat and tongue does not resemble the condition seen in scar- 
latina. Desquamation is often even more complete than in scarla- 
tina, and the hair and nails are frequently shed. Relapses are very 
common and give rise to the reported cases of repeated attacks of 
scarlet fever. 

Among other diseases in which rose rash appears we find diph- 
theria, septicemia, cholera, typhoid fever, malarial poisoning, and 
Bright's disease. In diphtheria it may lead the physician to a 
diagnosis of scarlet fever with severe faucial manifestations, and 
only a careful examination of the throat, the rapid subsidence of the 
rash, and the bacteriological examination of the false membrane will 
settle the diagnosis. Sometimes, however, a roseola appears late in 
the course of diphtheria, probably as a result of septic absorption. 
In other instances the injection of antidiphtheritic serum or other 
antitoxins produces this result. The presence of a very high tem- 
perature, of nervous irritability, and the predominance of the throat 
lesions of scarlet fever ought to decide the diagnosis in favor of 
scarlet fever. 

The physician should also recall the fact that the injection of 
antidiphtheritic serum sometimes causes a roseolous eruption, asso- 
ciated, it may be, with pains in the joints. The general illness caused 
by diphtheria, plus these symptoms, may point to a complicating 
scarlet fever or measles. The antitoxin rash is not, as a rule, so 
persistent as that of scarlet fever, lasts a short time, and is rarely 
followed by desquamation, except in fine scales. While it may 
resemble measles in its characteristics, the patient does not present 
the eruption on the pharyngeal mucous membrane nor the peculiar 
coryza of that disease, nor the bronchitis or other evidences of 
respiratory catarrh. 

The roseola of early syphilis resembles that of scarlet fever in 
that it first appears on the trunk; but it is not bright scarlet, but 
rather dusky red. It appears in patches and is not diffuse, and it 
ensues about six weeks or three months after the appearance of the 
initial lesion, occurs in an adult, as a rule, is not associated with 
high fever, and soon involves the face and forehead. These symp- 
toms aid us in separating it from scarlet fever, although the rash 



ERUPTIOXS ON THE SKIN HO 

often appears in full blast in the palms of the hands and soles of 
the feet; but a roseolous rash in these areas in an adult is always 
suspicious of specific trouble. These patches speedily change from 
rose rash to other more marked lesions in cases of syphilis, and one 
of the first changes that they undergo is to become circinate. They 
fade and reappear, last an indefinite time, fade in the centre, and so 
change into marginate or circinate erythema. 

When roseola develops after a surgical operation or after delivery 
in a puerperal female, it is not a manifestation of scarlet fever, but 
is due to sepsis ("surgical scarlet fever"), although it is, of course, 
possible for scarlet fever to attack such cases at any time. The 
rash is usually found over the abdomen and inner sides of the 
thighs. The absence of sore throat, the presence of a septic pro- 
cess, and the absence of a strawberry tongue all help to exclude 
.scarlatina. Sometimes late in an attack of cholera a rash like surgical 
roseola appears in the same areas, or in the period of reaction comes 
out on the forearms, backs of the hands, and rarely on the back. 

The roseolous rash of typhoid is sometimes widely distributed and 
almost like measles in appearance; but, as a rule, it is limited to a 
few or many rose spots on the abdomen chest, or back. These vo^v 
spots disappear on light pressure, but immediately return when the 
pressure is removed, and are most marked in typhoid fever about 
the seventh to the tenth day of the disease. They may become 
slightly papular. In this connection it should not be forgotten that 
the rose rash of typhoid fever may be so profuse, particularly in 
persons with a delicate skin, as to resemble scarlet fever; and, 
further, it is to be borne in mind that very rarely scarlet fever and 
typhoid fever may complicate one another. The abdominal symp- 
toms of typhoid fever and the throat symptoms of scarlet fever aid 
in the differential diagnosis. It should be remembered, however, 
that the exhaustion following an attack of scarlet fever may render 
the general appearance extremely like typhoid. In the relapse of 
typhoid fever the rose spots often appear as early as the third or 
fourth day. In typhus fever they are much more plentiful and often 
form petechia?. 

In B right's disease a roseola often appears over the feet and 
ankles, wrists and hands, and sometimes spreads to the skin of the 
chest and abdomen. Desquamation may take place, but absence of 
febrile movements and the presence of renal trouble render the diag- 
nosis easy. This manifestation has not a dangerous import. 

A dusky-red rash rapidly spreading over the neighboring skin, 
above the level of which the affected area is raised, and which is 
separated from the sound skin by a sharp line of demarcation which 
can be both seen and felt, is characteristic of erysipelas. The skin 
soon becomes brawny to the sight and touch, and the lines of demar- 



150 THE SKIN 

cation feel markedly indurated. Most commonly the disease ap- 
pears on the face, starting from the inner canthus of the eye. the 
nostril, or the corner of the mouth. Rarely erysipelas affects 
the skin of the trunk. The fever may be quite marked, even in 
mild cases, and usually falls by crisis on the sixth day. In severe 
cases with fatal tendencies there may develop in place of crisis a 
typhoid state with low fever and delirium. If the disease be severe, 
blebs and bullae form, edema of the skin becomes very profound, 
and finally suppuration may occur, forming what is known as 
phlegmonous erysipelas. (See also Glanders.) Erysipelatous inflam- 
mation of the skin without systemic disturbance may follow the 
application of arnica. A condition also closely resembling erysipe- 
las in its raised surface is urticaria, which, however, differs so mater- 
ially in other respects that a diagnosis is readily made. Aside from 
the absence of systemic disturbance in urticaria the swelling of the 
skin is not red, but pale and pearly in hue, although it may be sur- 
rounded by an erythematous blush; the onset is extraordinarily 
sudden, so that a skin seemingly normal at one moment, after a 
slight bruising by the finger or rubbing by the clothes, develops the 
complete eruption in a moment. 

A marked roseola or dermatitis involving the insides of the thighs 
or the scrotum or vulva should give rise to the belief that the patient 
is suffering from a failure to properly pass or retain the urine, which, 
on escaping, irritates the skin. This is particularly apt to result if 
the urine is that of a diabetic. 

It is an interesting fact that in some cases of tuberculous peri- 
tonitis an erythematous rash appears on the abdominal wall around 
the navel. 

The presence of a roseola or erythematous rash often indicates the 
untoward influence of some drug, following its external or internal 
use. We find that it very commonly follows the ingestion of copaiba, 
and, as many persons suffering from venereal disease take this drug, 
the physician must use care not to be led into a diagnosis of syph- 
ilitic roseola. It also follows the use of quinine, opium, antipyrine, 
and many other drugs, such as digitalis and chloral. 

The roseola caused by the use of copaiba appears by preference 
on the upper and lower extremities, and particularly on the backs 
of the hands, about the knees, the ankles, and on the chest, and it 
is often accompanied by fever. Indeed, the eruption caused by 
copaiba may closely resemble a papular syphilide; but its sudden 
onset, itching, and disappearance when the drug is stopped separate 
it diagnostically from the specific disease. 

The roseola following the use of bromide of potassium is, accord- 
ing to Veiel, very rare, and is distributed over the lower limbs. In 
children it may closely resemble measles. 



ERUPTIONS ON THE SKIN 151 

The roseola or erythema caused by quinine is to be separated from 
that of scarlet fever by the absence of fever, of the scarlet tongue 
and sore throat, and by the fact that there are no prodromes or cir- 
culatory disturbance except the characteristic evidence of cinchonism. 
In doubtful cases this is still further confirmed by analysis of the 
urine or by the use of the following simple test: Observe the dis- 
appearance of the fluorescence of the urine caused by quinine, after 
the sodium chloride has been removed by precipitation by nitrate of 
mercury, or after separating the quinine as an iodide by the addition 
to the urine of a solution of two parts of iodine, one part of iodide of 
potassium, and forty parts of water. The iodide of quinine can be 
again dissolved by the application of heat. 

A distinct diffuse roseola sometimes follows the use of arsenic. 
Roseola may be caused by the use of salicylic acid and strychnine, 
and a scarlatinifonn rash sometimes appears in blotches over the 
face and body in persons who are taking turpentine. 

Roseola also ensues in some persons after the application of sur- 
gical dressings containing iodoform, corrosive sublimate, and car- 
bolic acid, being due either to a local effect of these drugs or to their 
absorption from the dressings. Arnica tincture applied for sprains 
or bruises may produce marked roseola, or even erythematous and 
erysipelatous swelling of the skin, as already stated. 

An important drug exantheni is that caused by atropine, the rash 
produced by it being very like that of scarlet fever, except that it 
lacks the red punctations of that disease. This rash may be asso- 
ciated with a slight rise in temperature and be followed, rarely, by 
desquamation. The face of a child suffering from an overdose of 
atropine is very characteristic. The eyes are bright, the pupils 
widely dilated, and the skin over the malar bones is red, but striking 
lines of pallor reach from the corners of the mouth to the nose. 
There may be active, talkative delirium and very mild convulsions 
from overdoses of atropine, thus making the resemblance to the 
onset of scarlet fever very striking. The brief duration of the rash, 
its lack of punctation, the absence of high fever, and the history of 
the patient having taken atropine or belladonna, all help to make the 
differential diagnosis. 

Roseola, followed by desquamation, has been known to follow 
the hypodermic injection of mercury. Sometimes the use of blue 
ointment produces a widespread rash resembling measles, and this 
resemblance may be increased by the development of a febrile move- 
ment. A similar eruption may ensue from the ingestion of opium. 

Erythematous rashes, too, frequently follow slight irritation of 
the skin in persons who use chloral. 

Acne of the skin, particularly on the face, is often produced by 
the use of bromide or iodide of potassium, or of any preparation 



152 THE SKIN 

containing bromine or iodine. That produced by iodine is generally 
sudden in its onset and profuse in its distribution. The base of the 
pimple is bright red, the top speedily becomes pustular, and Fournier 
states that it may be hemorrhagic. Stopping the ingestion of the 
drug speedily relieves, or at least decreases, the eruption. The 
acne due to bromine is often very profuse, and the pimples in severe 
cases may coalesce, making sloughs of considerable size with an 
indurated base. 

In some persons, generally females, there is developed an acne 
on the face, breast, and back, as the result of taking iron as a tonic. 

In addition to the acne caused by drugs or their compounds, 
mention should be made of the acne and furuncles appearing in 



Fig. 43. — Smallpox eruption on the seventh day. 

persons working in paraffin, which is due to blocking of the sebaceous 
glands. 

Smallpox. — Closely associated with the eruption called acne is that 
which is characteristic of smallpox and chickenpox. The eruption 
of smallpox appears on the second or third day in the form of tiny 
specks, resembling flea bites. These rapidly become papules, which 
have an indurated base, so that they feel as if shot were under the 
skin (Fig. 43). After about thirty-six hours these papules become 
vesicles, containing a turbid fluid, which speedily becomes purulent, 
forming a pustule. Generally this process of maturation takes three 
days, and, with the development of the pus, the so-called secondary 
fever, which may be even higher than the primary fever of invasion, 



ERUPTIONS ON THE SKIN 153 

sets in. After a period of eighteen to twenty-one days the pustules 
drop off, having become dried up, leaving, if the attack has been 
severe or the skin delicate, deeply pitted scars. The vesicles of 
variola soon become umbilicated, are multilocular, and are difficult 
to rupture with the finger nail. Although the eruption of smallpox 
appears on the forehead, which is the favorite seat of acne in many 
cases, a differential diagnosis is not difficult, since the grave systemic 
disturbance, febrile movement, and rapid involvement of the skin 
of the limbs speedily indicate the true nature of the disease. The 
early appearance of the rash on the hands in variola is a valuable 
diagnostic sign, as acne in this part of the skin is practically unknown. 
Then the sudden development of the eruption in smallpox is entirely 
different from the gradual onset even of the most intense acne. 

It is not to be forgotten that cases of smallpox develop in which 
the symptoms of systemic disturbance are so mild that it seems impos- 
sible for true smallpox to be present, and also that acuminate syphi- 
lide accompanied by febrile movement may develop about six or 
seven months after infection, which may be accompanied by such 
marked systemic disturbance as to resemble smallpox. 

Pustular syphiloderm sometimes resembles smallpox so closely as 
to almost defy an immediate differentiation. The history of syphi- 
litic infection or of certain syphilitic eruptions, and the absence of 
severe systemic symptoms, may aid tis, but fever may be present. 
As the pock develops in syphilis it does not become so well umbili- 
cated, nor does it leave deep pits in the skin. 

In some cases a purulent acne of the forehead develops in 
syphilis. 

The separation of variola from measles has already been discussed, 
and it is only in the papular stage that the former disease can be 
confused with the latter, while the reddened mucous membranes and 
swollen face of the case of measles soon determine the diagnosis. 
The rapid formation of vesicles and the shot-like sensation of the 
eruption show that the rash is not measles. 

Vaccinia. — The appearance of the eruption of vaccinia following 
vaccination must be next described. Three or four days after the 
vaccination a single or several papules arise on the scarified surface, 
which by the sixth day are changed into umbilicated vesicles, which 
soon unite and form one vesicle the size of a five-cent piece. This 
vesicle finally forms a scab, which falls off after the expiration of 
about three weeks from the inoculation. A "good primary take" 
is always surrounded by an areola of rosy red of several inches in 
width. Rarely severe inflammation and sloughing ensue (Fig. 44). 
When the vaccination is a secondary one, the "take," if it occurs, 
often produces no symptoms until the ninth and tenth day, and the 
local lesions are then very mild. 



154 



THE SKIN 



Chickenpox. — In chickenpox the eruption appears on the first or 
second day, and keeps coming out for several days. It is rose- 
colored and occurs as papules, which immediately become vesicles. 
They last but four or five days, which is the time that it takes the 
eruption of smallpox to develop, and are usually associated with 
very mild febrile disturbance, the child remaining but little indis- 
posed if well cared for and nursed. Unlike smallpox, varicella does 
not become umbilicated unless it grows about a hair follicle which 





Fig. 44.— Typical vaccine vesicles of a "primary take." Tenth day. 

holds the centre of the pock, and rarely leaves pits in the skin unless 
the vesicles are picked at by the finger nails. Neither do the vesicles 
become pustules unless infected by picking or the child is in a con- 
dition of debility or suffers from struma. Varicella is separated 
from variola by the absence of severe systemic disturbance, by the 
rash first appearing on the chest and neck instead of the forehead 
and hands, by the presence of other cases of the disease in an epi- 
demic, by the repeated crops of the eruption in vaccinia, so that 
several sets of vesicles may be present at one time, and, finally, by 



ERUPTIONS ON THE SKIN 155 

the fact that it attacks children who have been well vaccinated, 
whereas smallpox does not. The history of exposure is, of course, 
an important point to be investigated. 

The profusion of the eruption is not of diagnostic aid, as it may 
be scant in variola and profuse in varicella. 

Impetigo. — An eruption somewhat resembling chickenpox or small- 
pox is that called impetigo contagiosa, in which there are found 
multiple, flattened or slightly umbilicated, roundish or oval vesicles, 
pustules or blebs, which form after some days dry yellowish crusts. 
It occurs in childhood or early adult life, and is often associated with 
some degree of fever. The areas involved are the face, neck, buttocks, 
hands, and feet. The lesions of the skin are larger than in chicken- 
pox, but often follow this disease. As its name indicates, the dis- 
ease is contagious, and the occurrence of a series of cases in close 
proximity to one another should not mislead the physician into a 
diagnosis of variola or varicella. The eruption lasts about two 
weeks, and Kaposi asserts that swelling of the submaxillary glands 
is always present. We can further separate impetigo contagiosa 
from varicella by the localization of its eruption to one area, as a 
rule, by the fact that the eruption becomes bullous or purulent, and 
by the larger size of the vesicle. From smallpox we can separate it 
by the absence of severe pain in the back, the grave systemic dis- 
turbance, and the secondary fever of that disease, accompanied as 
they are by the smallness of the pox, the peculiar odor of the patient, 
and the history of exposure to variola. 

In the presence of a papular, pustular, or vesicular eruption of 
the skin it must be remembered that quinine sometimes develops 
these lesions in susceptible persons. In some instances where it 
involves the hands it may indicate that a local effect has been pro- 
duced by working with the drug. 

Eczema in its various forms may appear as the result of the use 
of quinine internally or locally, or of the employment of mercury 
internally or externally. When it arises from the use of iodide of 
potassium, which is very rare, it chiefly affects the scalp and scrotum. 
The development of an eczematous irritation of the skin sometimes 
follows the use of chloral. 

Herpes Labialis is a very constant lesion associated with croupous 
pneumonia, and its development is said to be a favorable sign. It 
is also an important sign for the separation of epidemic cerebro- 
spinal meningitis from meningitis due to other causes, as it is not 
commonly present in the non-epidemic form. It sometimes arises 
as a result of using salicylic acid. 

The presence of herpes rather excludes tuberculosis, typhoid fever, 
and simple pleurisy from the case in instances in which the diagnosis 
is doubtful, since it is rarely met with in these maladies. 



156 THE SKIN 

In the cases of herpes zoster the skin lesion often has its origin in 
compression of the spinal cord, or in such diseases as tabes, spinal 
meningeal irritation, and peripheral neuritis. 

Furunculosis. — The development of recurring crops of boils in 
persons not exposed to paraffin or tar should cause the physician to 
suspect the presence of diabetes mellitus, or at least that there is gen- 
eral debility, and particularly an absence of lime salts from the system 
in the proper quantity. When the ordinary boil passes into a condi- 
tion of marked induration about its base, with sloughing of the subcu- 
taneous tissue and necrosis of the skin, which becomes perforated 
by the openings of several sinuses, we have to deal with a carbuncle 
or anthrax simplex. The disease usually appears on the back of 
the neck, on the back, or the lip. The systemic disturbance is very 
great and the exhaustion profound. The skin covering the area 
involved becomes grayish or bluish black, and then separates as a 
large mass, while the subcutaneous tissue comes away in shreds. It 
is a dangerous disease in all persons, but particularly so in those who 
are already weakened by other diseases or excess. 

Anthrax. . — The development of a painless macule on the skin of the 
hand or foot, followed by an acutely inflamed papule which itches and 
is soon changed into a relaxed vesicle containing bloody serum, in 
which there is a hard nucleus which rests upon an indurated base, 
is the initial manifestation of anthrax maligna or malignant pustule. 
The lymphatics soon become swollen, and metastatic abscesses 
speedily form elsewhere, as in the axillary glands. The systemic 
symptoms are severe, sometimes being manifested in high fever, in 
other cases by a typhoid state. Death is very commonly the sequel 
(65 per cent.), even if prompt surgical interference takes place. 
There is generally a history of exposure to infected animals or 
their hides. Malignant pustule is to be separated from carbuncle 
by its fulminating character and peculiar appearance. 

Glanders. — When an erysipelatoid rash with swelling of the skin 
and the development of papules, vesicles, pustules, and bullae appears 
in association with induration of the skin, with sloughing eventually 
taking place, the disease may possibly not be erysipelas of a phleg- 
monous form, but glanders or equina. Numerous inflammatory 
foci appear in the skin in glanders which end in local abscesses and 
hemorrhagic nodules, and profound systemic infection is always 
present. The presence of a sanious discharge from the nose aids 
in confirming the diagnosis. Death usually comes in a few days in 
this acute form. Should the course of glanders be chronic, pustules 
somewhat like those of smallpox, except that they are not umbili- 
cated, lie on an indurated base, and in them is formed a viscid or 
sanious pus of offensive odor. This disease is rare. Both forms 
arise from infection from a horse suffering from the malady. Glan- 



ERUPTIOXS ON THE SKIS' 157 

dcrs may be confused with variola or the pustular and ulcerative 
gummatous stages of syphilis. 

Pemphigus. — The development of pea-sized or larger bullae upon 
the skin may indicate the presence of pemphigus, or if there is central 
nervous disease involving the spinal cord and resulting in trophic 
lesions similar bullous eruptions may take place. The bullae, if they 
contain dark bloody fluid and are situated upon a limb in which there 
is an abnormally high temperature, are peculiarly indicative of cen- 
tral nervous lesions, particularly if there is a tendency to dilatation 
of the capillaries of the skin on slight irritation; but if the tempera- 
ture of the entire body be raised, the physician should remember that 
pemphigus is a disease in which there is often marked febrile move- 
ment. Sometimes these bullous manifestations are followed by 
gangrene in cases of neuritis or other disease causing trophic lesion-, 
such as myelitis and paretic dementia 

Bullae on the face may follow the ingestion of antipyrine or iodine 
compounds. 

The development of a pemphigus-like eruption in the skin may 
follow the use of salicylic acid or copaiba. 

Glossiness of the skin, in which its minute creases become smoothed 
out and it appears unduly shiny, often results from chronic disease 
involving some portion of the nervous system connected with 
the government of nutrition. Very commonly it results from 
peripheral neuritis. In addition to glossiness there are often redness 
and marked thinning or thickening of the cuticle and subcutaneous 
tissues. 

Gangrene of the skin may follow nerve injuries or central nervous 
lesions. Thus, it may follow upon division of a nerve trunk, or be 
due to cerebral abscess, in which case the gangrene will be with the 
other localizing symptoms on the opposite side of the body. The 
cerebral form develops suddenly and without the prodromal red- 
ness of bed-sores as seen in prolonged illness. Similar rapidly 
developing sloughs and ulcerations of the skin are seen in cases of 
acute myelitis and in the second and third stages of paretic dementia. 

A very interesting condition is the so-called spontaneous gangrene 
of hysteria. On the skin, generally of the breast of a young girl, 
a spot develops which feels to her to be hot and burning. The skin 
soon becomes very white, then in a few hours very red and forms a 
wheal. This rapidly becomes dark and bluish black, looking like 
a burn of sulphuric acid, and a slough finally comes away, leaving 
a permanent cicatrix. 

The development of gangrene of the fingers and toes sometimes 
follows the prolonged use of bread made from rye which is infected 
by ergot. 

Sometimes gangrene of the skin follows severe attacks of the 



158 THE SKIN 

exanthemata in children who are strumous or very feeble, or who are 
syphilitic. 

Ulcers about the base of the finger nails should arouse the suspicion 
of the excessive use of chloral. 

Bed-sores may develop whenever by long-continued pressure upon 
any part of the body the local circulation is disturbed, particularly 
if in addition there is general systemic debility from some exhausting 
disease, such as typhoid fever. They also develop very speedily, 
and apparently almost spontaneously, in the course of acute trans- 
verse myelitis. Under these circumstances the sacrum is the area 
most severely affected. Sometimes these sloughs have been known 
to develop as early as six hours after the beginning of the attack. 
Associated with the involvement of the soft tissues the bones may 
break down, and cellulitis about the rectum and bladder place the 
patient's life in immediate jeopardy. In hemiplegia, particularly 
in that which is due to cerebellar hemorrhage, bed-sores often form 
on the buttocks, and in paraplegia from other causes than transverse 
myelitis, upon the sacrum. They also appear on the heels, inside 
of the knees, and about the hips in some cases of paraplegia. 

Sudden sloughing of the skin of the nates sometimes occurs in 
cases of intracranial hemorrhage, and is said by Joffroy to be con- 
nected with lesion of the occipital lobes. 

Gangrene of the skin follows upon diabetes mellitus, and may 
involve the scrotum or vulva if the irritation of these parts by the 
urine is constant. More commonly the toes are affected, and there 
is this important differential point, that in the gangrene of old age 
with bad vessels the lesion is usually at the tip of the toe, whereas 
in diabetic gangrene it is frequently about the ball of the big toe or 
on the sole or dorsum of the foot. Previous to the development of 
gangrene there are developed bullae and other inflammatory changes 
in the skin which is about to be affected. Kaposi describes a ser- 
piginous form of gangrene affecting the leg in diabetics and a variety 
of tissue break-down in which a dermatitis, followed by ulcers and 
a lupus-like formation, also occurs in diabetes. Perforating ulcer of 
the foot occurs in locomotor ataxia and in paretic dementia. 

Raynaud's Disease. — Closely related, yet quite distinct from angio- 
neurotic edema, is that condition called Raynaud's disease, symmetri- 
cal gangrene, or local asphyxia, according to its severity. The fingers 
and toes or the nose, with or without exposure to cold, are found to be 
pale and livid, looking like a hand from which all the blood has been 
remo; ed by the use of an Esmarch bandage. The part often feels as 
if " asleep," and is more or less numb and without sensation. To the 
touch the part is cold and waxy, and it does not bleed when pricked. 
With the onset of these signs there are often general chilliness and 
malaise. Often this manifestation speedily disappears, leaving the 



ERUPTIONS OS THE SKIS 159 

skin apparently normal; but if it persists, the skin becomes glossy, 
shrivelled, and looks as if it had been soaked in hot water for hours. 
When the disease is more severe the pale waxiness is supplanted by 
cyanosis until the finger tips, for example, look as if dipped in blue 
ink; there is often local swelling; the skin is frequently found to be 
sweating freely and is distended with blood. The skin may rapidly 
separate from the deeper tissues and become necrotic in patches or en 
masse, and the entire tip of the finger, after becoming black, shrivels 
up into a condition resembling dry gangrene, which is separated from 
the sound skin by a sharp line of demarcation. Sometimes small 
necrotic patches slough out, which leave cicatrices telling of the 
attack. The prognosis is not bad. The most interesting compli- 
cation of the disease is paroxysmal hemoglobinuria. 

Rupia. — The value of roseola and rupial eruptions in the diagnosis 
of syphilis has already been dwelt upon. When the roseola becomes 
transformed into slightly elevated or bean-shaped spots, irregularly 
scattered, but sometimes forming groups which are apt to be circu- 
lar, and these circles become marginated and then scaly on the edges, 
resembling lepra or psoriasis, or even go further than tlii^ and 
develop bullae and blebs, and when the sores which form are filled 
with a clear liquid which may become sanious or turbid and on 
drying leave crusts, the removal of which reveals deeply excavated 
sloughs, the area of the slough often being as large as a silver dollar, 
but often irregular in outline, syphilitic rupia is probably the lesion. 
There is, however, this important differential point, namely, that in 
specific rupia there is an essential feature, a peripheral ring of indu- 
ration, whereas in the non-specific form this induration is absent. 

If, in addition to these variations, the eruptions are dusky red 
and leave behind them on healing copperish-looking discoloration 
of the skin, and appear on areas, such as the flexor surfaces, where 
ordinary skin eruptions are rarely seen, the diagnosis of syphilis is 
highly probable. If the eruption is chiefly tuberculated and the 
tubercles are large and more marked than usual, and if they ulcerate 
and become deep sores, and finally form on healing well-marked 
cicatrices, tertiary syphilis is to be considered the probable cause. 

If, again, we find small nodules under dusky-red skin, which 
finally breaks down and discharges bloody serum, or pus which in 
burrowing forms discharging sinuses, syphilis of the third stage 
may be regarded as a likely cause. 

The appearance of hard, dark-browm, infiltrated areas in the skin 
may be due to the excessive use of bromine, and as they gradually 
become depressed in the centre closely resemble in some cases the 
nodules of syphilis. 



160 THE SKIN 



SCARS OF THE SKIN. 

Scars of the skin often give us much useful information. Early 
tendencies to struma or tuberculosis may be found in the scars 
resulting from suppurating cervical glands. In the groin such 
scars may be an evidence of venereal infection, although it should be 
remembered that suppuration of these glands usually takes place 
as a result of chancroids and not from true chancre. It has 
already been shown that syphilitic skin lesions often leave scars 
to mark their site. Scars upon the head tell us of possible injuries 
to the brain in suspected traumatic epilepsy, or of falls in epileptics. 
Similarly, other traumatisms in the history of the patient may be 
discovered by scars elsewhere. 

The presence of numerous regularly arranged fine scars on the 
chest or elsewhere may develop the fact that the patient has at some 
time been wet-cupped for some pulmonary or other disease; or if the 
peculiar three-pointed scar of the leech is seen, another good evi- 
dence of a bleeding is presented. 

When the skin of the abdominal wall exhibits striae or scars 
arranged in parallel series, it indicates that it has been stretched 
very considerably by pregnancy, ascites, or, more rarely, by exces- 
sive corpulence. Sometimes these striae appear on the lower limbs 
in pregnant women or in persons with dropsy. Very rarely they 
may develop on the arms or legs or elsewhere during convalescence 
from some grave disease, such as typhoid fever. 



SWEATING OF THE SKIN. 

Sweating of the skin, aside from the normal and almost imper- 
ceptible exhalation of moisture, takes place in health as a result 
of severe muscular exertion, whereby the peripheral circulation is 
increased and the bodily temperature raised, or when the body is 
very heavily clad or exposed to external heat in excess. In all 
these cases the sweating is to be regarded as a physiological effort 
on the part of the body to reduce its temperature by increased 
evaporation from the surface. In disease sweating provides us with 
very important information in many conditions. 

During the course of fevers which naturally end by crisis the 
occurrence of a profuse sweat (generally associated with a fall of 
temperature) gives us the first sign of beginning convalescence, and 
in irritative fevers, or those due to cold and congestion, the artificial 
production of sweat is decidedly a good omen. The sweat of crisis 
is perhaps most marked in croupous pneumonia. Profuse sweating 



EXCESSIVE DRYNESS OF THE SKIN 101 

is also a characteristic symptom of relapsing fever, pyemia, acute 
ulcerative endocarditis, phthisis, malarial fever of the distinctly 
periodic type, and of typhoid fever and collapse. Constant profuse 
sweating is marked in some cases of acute articular rheumatism, 
and it is worthy of note that, while sweating generally occurs in 
febrile diseases at a time when the temperature is falling, in rheu- 
matism the febrile movement may even increase during the sweat 
rather decrease. 

Profuse so-called colliquative sweats often occur in sleep in debili- 
tated persons without the presence of any febrile movement, and are 
an evidence of profound nervous and vasomotor relaxation. Mod- 
erate sweating sometimes is seen from similar causes in feeble per- 
sons after taking anything in the food or drink which produces 
circulatory or nervous excitement. Localized sweatings occur 
almost solely in subjects of nervous disorder, which is often organic, 
as in paretic dementia, and sometimes functional, as in hysteria 
or Raynaud's disease. They depend upon perverted vasomotor 
influences sent to the glands and their supplying vessels in particular 
areas. Localized sweating of one side of the face or neck or chest is 
often a most important sign of a thoracic aneurysm pressing on the 
cervical sympathetic. Bromidrosis may occur in hysteria, or the 
head may be the only part affected in Graves' disease and in migraine. 
Profuse sweating of the head of an infant when sleeping may be 
indicative of rickets. In cases of the toxemia of cholera or of renal 
disease there may be profuse sweating, which takes the place of the 
dry and hot skin seen more commonly in this condition. The 
surface of the entire body is usually involved in the sweat. 

The quality of the sweat varies greatly in many persons. In 
cases of deficient renal activity it often contains urinary elements, 
smells uriniferous, and may even deposit particles on the skin in 
small white scales, particularly on the forehead and nose. This is 
called uridrosis. In jaundice the sweat may be bile-stained. 



EXCESSIVE DRYNESS OF THE SKIN. 

Excessive dryness of the skin is seen in grave forms of renal 
disease, in nearly all acute fevers with a high temperature, and in 
cholera and diabetes, in which diseases the dryness is largely the 
result of drainage of liquids from the body. Sometimes after a 
prolonged dryness of the skin during high fever, as soon as sweat- 
ing begins hundreds of little blisters develop, due to retained sweat 
under the epiderm. These are called miliaria or sudamina. 

When the skin is dry and harsh, and the naturally thickened por- 
tions have in their folds a peculiar white appearance as if filled with 



162 THE SKIN 

meal, diabetes should be sought for. Rarely the physician may be 
deceived by profuse sweating in diabetes, in which disease the skin 
is usually very dry. 



DROPSY AND SWELLING OF THE SKIN. 

Swelling of the skin and subcutaneous tissues occurs most 
frequently as a result of dropsy, in which condition the lymph 
spaces become filled by liquid. The skin in the area involved is 
not only swollen but doughy, or if the effusion is very great the 
skin may be of almost board-like hardness, so tensely is it dis- 
tended. Pressure with the tip of the finger upon such an area will 
result in pitting, and this is one of the more important signs 
separating dropsy or true edema from the swelling of acute 
inflammation, which, while it may be very tense, does not pit. 
Further, the swelling of inflammation is usually localized, reddened, 
and feels hot to the touch, whereas the dropsical swelling is more 
diffuse, is pale, and the temperature of the part is lower than normal. 

When the effusion of liquid is limited to one portion of the body 
it is usually called edema or localized dropsy, whereas if the entire 
body is boggy it is designated general anasarca. Dropsy is to be 
differentiated from myxedema by the facts that in the latter disease 
the onset is very slow, the swelling does not pit on pressure and is 
universal and fairly equally distributed over the body, the thyroid 
gland will often be found diseased, the subcutaneous tissues are not 
boggy but resistant, and there is anesthesia of the skin. When the 
subcutaneous tissues are distended by air, instead of liquid, they are 
even less resistant than in dropsy, the swelling is usually very local- 
ized and does not pit, and the part crackles or crepitates on gentle 
pressure. The presence of dropsy is indicative of many widely sepa- 
rated diseases. In the first place, it may indicate a deficient circu- 
lation of blood, either by reason of a feeble or diseased heart or because 
of obstruction by the pressure of growths, thrombi, or emboli. 

It may be due to disease of the walls of bloodvessels and lym- 
phatics, as is generally the case in renal disease, or it may arise from 
disease of the blood itself. Again, in some cases it is due to dis- 
ordered nervous control of the vessels, by reason of centric or 
peripheral changes which may be organic or functional. 

General Anasarca. — The significance of a widely diffused general 
dropsy or anasarca is generally that there is well-marked renal disease, 
and this probability is greatly strengthened if the edema of the face 
be well marked, particularly in the morning on arising, disappearing 
as the day goes on. The skin in such cases will usually be quite 
pale, and an examination of the urine will reveal the presence of the 



DROPSY AND SWELLING OF THE SKIS 163 

signs of nephritis. The next most common cause of general ana- 
sarca after renal disease is heart disease. When due to this cause 
it will be found that the ghastly pallor of renal anasarca is replaced 
by cyanosis, and often by engorgement of some of the superficial veins, 
while the physical signs of cardiac disease will confirm the diagnosis. 
General anasarca may rarely arise as a result of a multiple peripheral 
neuritis, and it also occurs as a symptom of beriberi and from the 
excessive use of large amounts of arsenic. This arsenical anasarca 
may be due to the neuritis produced by the drug, although Wood 
thinks it is due to a cellulitis. Rarely we find general anasarca in 
cases of advanced cancerous cachexia, and care must be exercised 
that the hemic murmur due to anemia does not mislead the physi- 
cian into a diagnosis of heart disease. 

Local Dropsy. — The most common seat of localized dropsy or 
edema is the feet and legs, particularly about the instep, the ankles, 
and the tibiae. When it is bilateral it is generally indicative of 
cardiac failure or more rarely of renal disease. Nearly always, if it 
be renal, a careful examination will discover edema in other parts 
of the body, although it may be most marked in the feet and legs. 
In many cases the various serous sacs, such as the pericardium, 
peritoneum and pleurae, will be found to contain more liquid than 
normal, and the tissues generally will be found infiltrated. 

Other causes of edema of the feet and legs are anemia, and 
obstruction to the return of blood from the lower limbs by reason 
of growths in the abdomen pressing upon the iliac veins or inferior 
vena cava. Thus, cancer of the pancreas sometimes causes edema 
of the feet and legs in this manner. Very rarely edema of the 
lower extremities follows hepatitis or hypertrophic cirrhosis of the 
liver as a primary symptom. Usually such lesions produce ascites 
alone, or if the legs are involved they become so by reason of the 
pressure of fluid in the pelvis during the time that the patient is 
sitting up or standing. This latter cause of bilateral edema of the 
lower limbs is, however, rare. Sometimes edema of both legs and 
feet comes on in persons who, though feeble and relaxed, remain 
standing with little muscular movement during many hours in the 
pursuit of their occupation, as in typesetters and salesmen, or in 
young persons who have subjected themselves to excessively severe 
muscular exercise. In other instances, very much more frequently, 
edema of the feet and legs comes on in the course of profound 
anemia resulting from slow hemorrhages or other causes. It is 
also seen in the cachectic stage of cancer, owing to the anemia which 
is present. General swelling of a leg in a puerperal woman is prob- 
ably due to phlegmasia alba dolens, and this affection may also be 
bilateral. Both Herman and Cameron Kidd have each reported a 
case of bilateral phlegmasia alba dolens occurring in a virgin with 



164 THE SKIN 

anemia. When it occurs in males it is most commonly unilateral 
and a complication of convalescence in typhoid fever. It is due to 
thrombosis of the left femoral vein, as a rule. 

Dropsy diffused or localized in the feet and legs occurs in scurvy. 

When the face is edematous the swelling is most marked under 
the eyes, the lower lids of which are particularly puffy in the morning 
and nearly normal in appearance at night. This form of edema 
is most marked in, and is almost pathognomonic of, renal disease. 
Its only other causes are the excessive taking of arsenic and angio- 
neurotic edema. More alarm should be felt at a slight swelling of 
the face of this character than if the feet are markedly puffed. 
Sometimes edematous swelling of the side of the face and scalp which 
has been involved in a severe attack of neuralgia takes place. 

When edema of one or both eyelids occurs, with protrusion of the 
eyeball, the swelling extending to the rest of the face as time goes on, 
it forms an important symptom in obscure cases of suspected cere- 
bral thrombosis, and is caused by the intimate association between 
the intracranial vessels and those of the face. 

Sometimes edema of the eyelids comes on in neurotic subjects and 
may extend to the forehead. This may be seen in children, most 
commonly about puberty, and is probably the result of a neurosis. 

Edema of the upper extremities alone only results from causes 
interfering with the flow of blood, such as are produced by morbid 
growths in the chest, as mediastinal growths, and in cases of aneu- 
rysm. When the swelling is limited to one arm or leg it is a sign 
that there is interference with local circulation, as, for example, the 
obstruction of the femoral vein by thrombus, as in phlegmasia alba 
dolens following labor or enteric fever, or, when the edema is in 
the left leg, by cancer of the sigmoid flexure. If the swelling of 
the arms and head is manifested suddenly, it may be due to that rare 
condition in which an aortic aneurysm ruptures into the vena cava ; 
whereas if it develops slowly, it is due to pressure by a growth. 

There remain three forms of local edema of some diagnostic sig- 
nificance, namely, that occurring in a limited area over some deep- 
seated suppurative process, as in the skin back of the ear in cases of 
mastoid abscess or thrombosis of the lateral sinuses, that over the 
ribs in cases of purulent exudation into the pleura, and that on the 
thigh in the abscesses which sometimes follow typhoid fever. 



ADIPOSIS DOLOROSA. 

No better place can be found in which to mention that condition 
in which irregular and numerous masses of fat are to be found in 
the subcutaneous tissues of middle-aged persons, usually women; 



SENSATION IN THE SKIN 165 

these masses are more or less painful, and occur id the body 
and extremities. The skin itself is not altered. Dercum first 
described this state and gave it the name of adiposis dolorosa. 

The ocular appearance and touch of the skin having been studied 
in so far as its surface affords evidence of more deeply seated disease 
or functional disturbance, we next pass to a study of its sensibility, 
having the same diagnostic objects in view 



SENSATION IN THE SKIN. 

Before considering the various perversions of its sense it is im- 
portant to remember that the sensibility of the skin may be 
divided into four parts, namely, its tactile sense, its pain sense, 
its thermic sense, and its sense of pressure. Any one of these 
senses may be perverted or in abeyance without the others being 
affected, and it is noteworthy that, while corresponding areas of 
the skin in all individuals have practically identical sensibilities, 
each part of the skin has a sensitiveness of its own, so that 
while in some parts the slightest touch is felt, in others severe 
irritation must be produced to cause much of a result. These 
differences have been carefully sttidied by many observers, the 
most thorough being Weber, who has found that the average 
ability to separate points brought in contact with the skin is 
about as follows: at the finger tips points can be separated at from 
2 to 3 mm., on the lips 4 to 5 mm., on the tip of the nose 6 mm., 
on the cheeks and backs of fingers 12 mm., and on the forehead 
22 mm. 

The skin on the neck separates points at 34 mm.; that on the 
forearm, on the lower leg and back of foot, at 40 mm.; on the 
chest at 45 mm.; on the back at 60 mm., and on the arm and 
thigh at 75 mm. If tests be frequently repeated in a single indi- 
vidual, the ability to separate the points increases with training. 
Care should always be taken that the pressure on both points is 
equal, applied simultaneously, and that the points are equally 
sharp. 

In testing tactile sensibility, not only should points be used, but 
also objects. Often single points may be applied without any 
abnormal manifestation, and, in some cases of disease, the skin, 
which seems devoid of sense on ordinary touch, is found to be 
excessively hyperesthetic if the hand is drawn lightly over it. 

The best apparatus for testing tactile sensibility is the esthe- 
siometer of Carroll, which is a pair of double-pointed compasses 
connected by a graduated scale. (.See Fig. 45.) 

The ability to distinguish pain-giving and thermal applications is 



166 



THE SKIN 



most acute in the normal skin of the hands, in which tactile sense is 
also most acute. 

The methods by which we test the pain sense are several, bu 
chiefly by pricking the skin, more or less deeply, with some sharp 
pointed instrument, such as a pin, or by pinching the integument. 

The thermal sense is studied by applying bodies which are hot or 
cold against the skin, such as a cold knife, a small piece of ice, or a 
test tube which contains very cold or hot water. In all such tests 
the physician should use both hands simultaneously. With one 
hand he should apply his instrument to the suspected area, and with 
the other a similar instrument to an area known to be healthy, in 
order that an actual comparison as to the sensations may be noted 
by the patient. Thus the face may be used 
as the normal area in a spinal lesion, and 
the skin of the arms as a control surface in 
a lesion involving the legs. The eyes of the 
patient should be blindfolded, and if tactile 
sense is being tested the instrument must be 
of the same temperature as the body. 

Closely connected with the subject of tactile 
sense is what is known as stereognosis, or the 
ability to recognize objects by contact and 
grasp. By this means healthy persons are 
able without looking at an object to judge of 
its character, and in the blind this sense is very 
highly developed. Manifestly the entire sen- 
sory apparatus must be intact for stereognosis 
to be performed, since any interference with 
the sensory system will produce that condi- 
tion which is known as "astereognosis." 
Not only does stereognosis involve the tactile 
sense but also muscle sense, since it is by the grasping of the object 
that information concerning it is gained, as well as by its coming 
directly in contact with the hand. At the present time the discovery 
of astereognosis in a patient has not very definite clinical significance, 
so far as localization of the lesion producing this condition is con- 
cerned, but when astereognosis does not depend upon a disease of 
the sensory nerves, it depends upon involvement of the cerebral 
cortex, in the middle third of the posterior central convolution and 
in the adjacent part of the inferior parietal lobule. Of course, it is. 
possible for a lesion in the sensory fibers of the internal capsule 
to cause astereognosis; but a lesion of any size in this region will 
usually produce signs of motor paralysis, owing to the juxtaposition 
of the motor and sensory fibers. 

Disturbances in the sensation of the skin may arise from functional 



= 




45. — Carroll's esthesi- 
ometer. 



SENSATION IN THE SKIN 



107 



or organic disease involving the peripheral nerves, the sensory 

tracts in the spinal cord, similar tracts in the lower part of the 
brain, and, finally, the subcortical or cortical parts of the cerebrum 
itself. 

The sensory pathway or the afferent fibers pass upward, starting 
with the peripheral sense organ in the skin, or elsewhere, and after 
forming part of the nerve trunk and entering the ganglion on the 
posterior root, enter the spinal cord by what is called the posterior 
root, which is shown in Fig. 40. 




Fig. 46. — Columns of the coul. (Gray.) 



The posterior root enters the cord in three sets of fibers; one of 
these, the one lying nearest the posterior median fissure, is composed 
of coarse fibers and is called the median bundle, and passes obliquely 
into the lateral part of the column of Burdach. As soon as they have 
entered this column they turn at right angles and run upward for 
some distance, thereby helping to form the column of Burdach. 
Some of them also run downward a short distance. Some of these 
fibers also enter the column of Goll. 

The second set, near the side of the cord, goes directly into the 
gray matter of the posterior horn through the substance of Rolando, 



108 THE SKIN 

and the third set, nearest the side of the cord, enters the cord very 
superficially, and, turning at once at a right angle, goes upward to 
form Lissauer's zone. Here they pass upward chiefly in the column 
of Goll (posterior median) to the medulla oblongata. Before 
reaching the medulla, however, the column of Goll ends in the 
gracile nucleus and the column of Burdach in the cuneate nucleus. 

These nuclei which have received the fibers of the two. sensory 
columns give origin to fibers which pass to the brain. They sweep 
forward to the front of the central canal of the medulla and decus- 
sate at a higher level than the motor tracts. A great majority of 
these fibers pass upward to the brain, but some pass forward, and 
finally join the restiform body on the posterior aspect of the medulla. 
Those which pass upward from the so-called fillet pass into the 
crus cerebri, in that part of it called the tegmentum, and thence 
into the posterior part of the posterior limb of the internal capsule, 
whence they spread out in the corona radiata to the occipital lobe 
and temporosphenoidal lobes. 

The duty of the physician in all cases is to determine first whether 
the disorder of sensation is functional or organic, and then where 
the lesion producing the symptoms is situated. 

The two chief manifestations of perverted sensibility in the skin 
are anesthesia and hyperesthesia, and the minor ones are pares- 
thesia or numbness, tingling and formication, and analgesia, or the 
failure to feel pain. Whatever the cause of these symptoms may 
be, the history of the patient and his general symptoms should be 
carefully studied when examining these signs, as frequently a diag- 
nosis is impossible with them alone as guides. 

Anesthesia. — Anesthesia of the skin is indicative of a very large 
number of conditions arising anywhere in the sensory apparatus. 
In other words, anything which interferes with the transmission of 
an impulse to the perceptive centres in the brain may be its cause. 
Of the functional causes, the most frequent is hysteria, and the 
presence of cutaneous anesthesia in a female should always arouse 
a suspicion of its being due to this cause. Rarely it is seen in hys- 
terical males. The organic causes of anesthesia of the skin are 
cerebral hemorrhage, cerebral tumor, hemorrhage in the pons or 
tumor of the pons, hemorrhage in the cord, tumor of the cord, mye- 
litis (transverse), locomotor ataxia, cerebrospinal meningitis, spinal 
meningitis; compression of the cord by vertebral caries, by frac- 
tures, by dislocations; and hemorrhage into its membranes. Addi- 
tional causes are pressure on the posterior nerve roots by reason of 
caries and growths, inflammation of the nerves (neuritis), injuries 
to the nerves by blows, pressure, or cutting, and, finally, by paralysis 
of the nerve endings from cold or the action of drugs. 

Anesthesia, according to its area of distribution, may be divided 



8E VSATION IN THE SKIN 169 

into hemianesthesia, crossed anesthesia, bilateral anesthesia, irreg- 
ular but complete anesthesia, and partial anesthesia. 

Hemianesthesia occurs most frequently as a result of hysteria, 
next commonly from lesion of the posterior part of the internal 
capsule, and more rarely from spinal injuries or growths in the cord 
of a unilateral character. 

The hemianesthesia of hysteria involves, as its name implies, one 
side of the body, and is usually universal on that side, except that 
here and there may be patches of hyperesthesia or tenderness, dotted- 
like oases in the midst of the absence of sensation. This anesthesia 
is often unaccompanied by motor paralysis, and its area is separated 
from the opposite side of the body by a sharp line of demarcation, 
which runs along the middle of the trunk and face. The presence 
of such a well-defined line of separation in a young woman is of 
great significance. The anesthesia is generally absolute, and severe 
injury may be done to the skin in some cases without the patient 
feeling it; but, notwithstanding its degree, it is a noteworthy fact 
that the anesthesia may transfer itself to the opposite side of the 
body with great suddenness, and equally suddenly return to it^ 
former site. In a great majority of cases, for some unexplained 
reason, the left side is the one affected by anesthesia, and hyperes- 
thesia on the opposite side increases the contrast which exists between 
it and that in which sensation is lost. (See Hyperesthesia.) In 
some cases of hysterical hemianesthesia the paralysis of sensation 
involves the nerves of special sense; and loss of smell, taste, and 
hearing, and impairment of sight may ensue on the same side. The 
visual changes are so characteristic that they practically decide the 
character of the case when they are discovered in any instance of 
doubtful diagnosis; they consist in a loss of the color vision (first, 
violet is lost, then blue, and then red), and there is a great limitation 
of the visual field, whereas in the hemianesthesia due to an organic 
lesion in the internal capsule, so situated as to involve the nerve 
fibers connected with vision, there is hemiopia. Hemianopsia due 
to hysteria is so rare as to be denied an existence by most authori- 
ties, but Lloyd and de Schweinitz have seen a case. Generally the 
loss of vision on the anesthetic side is a total one for both sides of 
the eye in hysterical blindness. (See chapter on the Eye.) Nearly 
always in hysterical hemianesthesia a spot can be found over the 
shoulder which is not anesthetic. The age of the patient, the sex, 
the general expression of the face, and the history of the illness, 
associated, as is frequently the case, with some or all of the hysterical 
symptoms detailed farther on in this chapter, will generally decide 
the diagnosis in favor of hysteria. 

A form of hysterical hemianesthesia very apt to lead to an error 
in diagnosis is that seen in persons who have suffered from infantile 



170 THE SKIN 

cerebral paralysis with the resulting deformity (a disease not char- 
acterized by sensory disturbances), but who have in later life, 
superimposed upon the old picture of disease, that of hysteria with 
this sensory manifestation. 

Anesthesia irregular in its distribution, or absolute hemianes- 
thesia, may occur in the course of chorea. The presence of the motor 
manifestations of chorea clears up the diagnosis as to the cause of 
the loss of sensation. 

Hemianesthesia when not hysterical is nearly always due to an 
organic lesion in the posterior part of the hinder limb of the internal 
capsule on the opposite side of the brain from the anesthesia, and 
the additional symptoms which sometimes accompany it depend for 
their existence upon whether the lesion is large enough to involve 
not only the fibers from the cutaneous areas, but also those of special 
sense, such as sight, hearing, or taste. Nearly always the area de- 
stroyed is sufficiently large to result not only in hemianesthesia, but 
also in loss of motion on the same side. The loss of sensation in 
such a case is rarely as complete as in hysteria, and the sole of the 
foot and palm of the hand are often not affected. In rare instances, 
however, the hemianesthesia of capsular disease may be absolute 
and universal, or, more rarely still, occur in patches, thereby closely 
resembling the anesthetic areas seen in hysteria. 

Hemianesthesia may also be produced by a large lesion of the 
cortex in the occipital, temporal, and parietal lobes, in which case it 
will involve the side of the head as well as the trunk, and will be 
associated with such definite evidences of apoplexy or injury that 
the diagnosis will be readily made. If it is widespread, all the 
special senses will be involved. 

Sensory disturbances of the skin are. more frequent in softening 
of the brain than in hemorrhage into the brain, and most commonly 
are associated with subcortical, rather than cortical lesions. 

In this connection it should be remembered that the irregularity 
of distribution of the lesions in disseminated sclerosis may cause a 
hemianesthesia, partial or complete. 

Anesthesia resulting from tumor of the brain occurs in about 20 
per cent, of the cases, and may be unilateral and confined to the 
paralyzed side, or appear as an isolated symptom without motor 
paralysis. When of the latter form it is often associated with lesions 
in the neighborhood of the fissure of Rolando, and in tumors involv- 
ing the posterior parietal region and the posterior part of the internal 
capsule. 

Autopsies and experiments show that hemianesthesia may arise 
from a lesion in the optic thalamus, but such an occurrence is very 
rare. 

A very important and essential factor in making the diagnosis 



SENSATION IN THE SKIN J 71 

that the anesthesia is cerebral in origin is the history of the beginning 
of the attack, which has been sudden if due to hemorrhage, embolus, 

or thrombus (see Hemiplegia), and characteristic of the condition 
which we call apoplexy. 

An important point to be noted in the diagnosis of cerebral anes- 
thesia is the fact that the reflexes are preserved, though the patient 
may not feel the touch or painful impression; that is to say, irrita- 
tion of the skin causes movement in the arm or leg, not by any 
intention of the patient, but owing to the fact that the sensory centres 
in the cord receiving an impulse cause the corresponding motor 
centres to send out impulses which contract the muscles. 

Unilateral anesthesia associated with motor paralysis, both being 
somewhat irregular in their distribution, may be due to a lesion, 
such as a tumor in the pons or medulla oblongata, but death so com- 
monly ensues soon after the apoplexy that the symptom is often 
overlooked or cannot be developed when this accident is the cause. 
Further, the discovery of such anesthesia does not positively localize 
the lesion in the pons, for we do not know much about the course 
of the sensory fibers in this part. If, however, the area supplied 
by the trifacial nerve, namely, the face, is anesthetic, and these 
symptoms are associated with it, then it is fair to assume that the 
trouble lies in the pons and has involved the nucleus of the fifth 
nerve. (See Anesthesia of the Face.) 

Anesthesia of irregular distribution or confined to one limb may 
result from cerebral or spinal lesions, or be due to a neuritis, of 
which we shall speak farther on. If it is a mono-anesthesia from 
cerebral disease, which is very rare, the anesthesia is most marked 
at the distal part, and gradually fades off as the trunk is approached. 
It is evenly distributed, so far as circumference is concerned, and 
has no sharp line of demarcation. 

When such an anesthesia is due to spinal disease the cause may 
be tumor of the spinal cord, the symptoms depending in their char- 
acter on the area involved; but in any event the upper border of the 
area involved is sharply outlined and a constriction-band sensation 
is often present. 

The irregularly distributed form of anesthesia due to hysteria 
has the same general peculiarities of migration as are seen in hemi- 
anesthesia from this cause, and in its symmetrical form it closely 
resembles the anesthesia due to multiple neuritis. Thus, in the 
hand the area of anesthesia may be that covered by a gauntlet 
glove, in the foot that covered ordinarily by a sock, the line of 
normal sensation being present just above the place to which these 
protections usually extend. 

Crossed Anesthesia. — When sensory paralysis of one side, asso- 
ciated with partial paralysis of motion or paresis on the same side, 



172 THE SKIN 

comes on, and with it there is hyperemia of the skin on that side 
from vasomotor paralysis, there is a strong probability that there 
is a lesion in the cerebral peduncle of the opposite side. If there is 
at the same time paralysis of the muscles supplied by the oculomotor 
nerve on the opposite side from the anesthesia — that is, on the same 
side as the lesion, this diagnosis is still further confirmed; and if 
the tongue and half of the face on the anesthetic side of the body 
are paralyzed, still further confirmatory evidence of a peduncular 
lesion is obtained. Thus, there might be hemianesthesia and par- 
alysis of the right side of the body, including the face and right half 
of the tongue, and ptosis, from oculomotor palsy, on the left side of 
the face. The paralysis of the body, face, and tongue would be on 
the side opposite to the lesion, but the oculomotor paralysis would 
be on the same side as the lesion. 

Crossed anesthesia of the limbs and face — that is, anesthesia of 
one side of the body with anesthesia of the opposite side of the face 
— can only occur in lesions involving the upper part of the pons in 
such a way that the fibers of the trifacial are diseased on one side, 
and the path for sensory impulses of the other side of the body is 
also destroyed. (See chapters on the Face and Head, and on Hemi- 
plegia.) 

Partial hemianesthesia, with partial hemiplegia on the opposite 
side in crossed paralysis, may occur from lesions on one side of the 
spinal cord, and if high up, involve a large part of the trunk and 
lower limbs. (See chapter on the Feet and Legs, part on Myelitis.) 
These cases have been explained by a theory of Brown-Sequard, 
which has recently been doubted owing to the studies of Mott and 
others. Thus, until recently it was considered as proved that sen- 
sory impulses entering the cord crossed to the opposite side almost 
at once, at least in greater part, passing to the lateral columns in 
front of the pyramidal tract, and that a very small number entered 
the posterior columns, while a few ascended in the gray matter. 
The studies of Mott seem to prove that the reverse is the case, and 
that the greater part of the sensory impulses do not cross the cord, 
only a few fibers passing to the opposite side on entrance. He 
believes that the main pathway for heat and cold sensations is in 
the gray matter, while the tactile pathways are in the posterior 
columns, although it is possible that some few isolated fibers may 
exist in the lateral columns and that these cross in the cord about 
the level of entrance. 

Bilateral Anesthesia. — Anesthesia of hysterical origin involving 
both legs, and sometimes the lower part of the trunk on both sides, 
may occur, and, aside from the typical signs of hysteria in general 
which distinguish it, may be discovered by the fact that in hysteria 
the failure of sensation does not involve the skin of the genitals, as 



SENSATION IN THE SKIN 173 

it does in organic lesions producing somewhat similar symptoms. 
In addition it will be found that in hysteria a V-shaped piece of 

skin over the sacrum is not anesthetic. Anesthesia of this variety, 
corresponding in the sensory organs to what we call paraplegia in 
the motor apparatus, is practically never produced by a cerebral 
lesion, and, if not hysterical in cause, must be spinal; but it is much 
more rare than is motor paralysis in these parts from lesions in the 
spine. When it does ensue from spinal causes motor paralysis 
will in the great majority of cases be found associated with it, at 
least to some extent. To express it concisely, the characteristic of 
a typical spinal anesthesia is that it is bilateral and usually involves 
both sides quite symmetrically; that motor paralysis is generally 
associated with it; that the reflexes are greatly perverted; and that 
trophic changes may be present as a result of an involvement of 
the trophic cells in the anterior cornua coincidently with the disease 
of the sensory parts of the cord. 

The diseased conditions of the cord which result in symmetrical 
anesthesia of the skin of the legs and trunk are, first and mosl 
prominent, locomotor ataxia; second, myelitis; hemorrhages, tumor 
of the cord or its membranes, meningitis, or injuries which cause 
pressure on the sensory tracts by producing fracture of the vertebra' 
or dislocation. Very rarely, however, a lesion of the pons may so 
result. 

Anesthesia of the lower "portions of the bod// and legs occurs in 
the later stages of locomotor ataxia, and is usually preceded by forms 
of paresthesia. (See Paresthesia.) The anesthetic areas are mosl 
marked in the soles of the feet and about the malleoli, according to 
Belmont. In other words, blunting of sensibility is seen in nearly 
all cases of tabes dorsalis late in the disease. In some cases the 
sense of touch is preserved and the sense of pain lost (analgesia), 
while in others the opposite condition is present. Again, we find 
loss of tactile sense and of pain sense without loss of heat and cold 
sense, and vice versa. A very characteristic sensory symptom of 
tabes is the delay in the recognition of an irritation of the sensory 
nerves, so that if the patient be blindfolded and then pricked with 
a pin he will not make an exclamation or draw his foot away for 
several seconds. In other instances the patient complains of re- 
peated pricks when only one has been given, or, when asked the 
number of points pricking him, states that there are four or five 
instead of the one really present. If, in addition to these sensory 
disturbances, we find Romberg's symptom (see Legs), Argyll- 
Robertson pupils (see Eye), and loss of patellar reflex (see Reflexes), 
and a number of other diagnostic peculiarities of tabes, the decision 
as to the cause of the anesthesia is easily made. 

An important early diagnostic sign of locomotor ataxia is the 



174 THE SKIN 

development of areas, unilateral or bilateral, of diminished sensi- 
bility. This is particularly apt to be found in the areas supplied by 
the mid-dorsal nerves (level of fourth intercostal space). They are 
very constant symptoms. When the disease is advanced the anes- 
thesia extends down the inside of the arms and forearms. The 
sense should be tested by a warm finger tip applied to the skin in 
a very gentle manner. 

Slight anesthesia, retardation of the transmission of sensory 
impulses from the skin, and perversion of temperature sense may 
be rarely developed late in the course of Friedreich's ataxia. 

Bilateral anesthesia of the character just discussed, as caused by 
locomotor ataxia, may also occur as a result of acute or chronic 
myelitis. The first change under these circumstances is a mere 
obtunding of sensitiveness, which gradually deepens until loss of 
pain sense, pressure sense, and, lastly, complete anesthesia is devel- 
oped. The development of these symptoms indicates involvement 
of the posterior columns. Loss of reflex activity in the legs is 
developed in direct proportion to the destruction of the motor and 
sensory nerve tracts in the cord. The predominance of motor 
paralysis, the fact that the lower limbs are both involved, and the 
absence of the characteristic symptoms of locomotor ataxia all tend 
to make the diagnosis certain, while the absence of the pains of 
tabes and of the other signs of that disease still further excludes its 
presence from the case. Further than this, the myelitis creeps up 
the cord, involving new areas, and new parts of the skin become 
anesthetic. An important point, too, in regard to the anesthesia 
of acute myelitis is this, namely, that while in the upper extremities 
the loss of sensation and motion is associated, so that both functions 
are lost in the same area, in the lower extremities these two functions 
are not lost in the same areas. Thus, myelitis of the lumbar enlarge- 
ment in its lower part is accompanied by anesthesia of the gluteal 
area and motor paralysis of the anal muscles; and, again, anesthesia 
of the gluteal region, the back of the thigh, and the back of the calf 
is associated with loss of power in the muscles that move the foot, 
while in lesions of the upper part of the lumbar segment the anes- 
thesia involves the thigh, the inner side of the leg, and the foot, in 
association with paralysis of the quadriceps extensor and deeper 
muscles of the thigh. (See chapter on the Feet and Legs, part on 
Myelitis.) 

The development of sudden bilateral anesthesia, which is accom- 
panied by severe pains of a tearing or burning character, creeping 
rapidly up the body, is indicative of acute hemorrhage into the 
spinal membranes, or it may be due to that very rare lesion, hemor- 
rhage in the cord. In either case motor paralysis is present. Anes- 
thesia, or the milder perversions of normal sensibility of the skin, 



SENSATION IN THE SKIN 



1.75 



may be present in cases of compression of the cord by caries, and 
by spinal curvature, tumors, or aneurysms producing erosion. Some- 
times, while; tactile anesthesia is complete in these cases, severe pain 
is constantly suffered (anesthesia dolorosa), and this is often the case, 
according to Wood, in cancer of the spine. 

Partial anesthesia of the skin of the trunk and arms of a bilateral 
character, associated with progressive muscular atrophy, scoliosis, 
and trophic lesions in the skin, points strongly to syringomyelia. 
The loss of pain and temperature sense is usually the first symptom. 
The areas of anesthesia are best shown in Fig. 47. 



Fr<;. 4" 



Sensory chart, showing 
areas of . . . . 




Analgesia & f\Thenno-Anaesthesia 
■» and Analgesia 



J Titer mo- Anaesthesia 
Tactile Anaesthesia , and areas in which the patient's answer to tests of temperature 
showed reversal 



Hot-Cold. m a case ° f s . vl ' n g omvelia - (Dercum.) 



Localization of the Spinal Lesion. — Having considered the general 
spinal causes of anesthesia of the skin, it yet remains to determine 
what part of the cord is involved by the pathological process; and 
this is, fortunately, possible, chiefly through the very accurate and 
noteworthy studies of M. Allen Starr, Thorburn, and Head, not to 
mention collateral ones of great value by Horsley and many others; 
but the field is only partly covered, and some of our uncertainties 
depend upon lack of knowledge as to the course of the sensory fibers 
in the cord. 



176 



THE SKIN 



Roughly, we may state that disease of the cervical cord generally 
produces disturbances of sensation in the arms, hands, and fingers; 
disease of the dorsal cord, disturbances in the sensation of the back 
and trunk, which may radiate into the thighs; and disease of the 
lumbar cord gives rise to these symptoms in the legs and feet. 

Again, it is to be remembered that, as a rule, in a transverse 
lesion of the spinal cord the anesthesia begins at a level which is 
three or four inches below the lesion in the cord (Horsley and 
Gowers) ; this being due, as proved by Sherrington, to the fact that 



8th cervical and 1st dor 
sal segment at 7th ver 
tebra. 



Lumbar enlargement of 
cord at 10th dorsal ver- 
tebra. 



End of cord at 2d lumbar \ 
vertebra. 



Cauda equina 




1st to 7th cervical 
vertebra. 



1st to 12th dorsal 
vertebra. 



1st to 5th lumbar 
vertebra. 



1st to 5th sacral 
vertebra. 



Fui. 



48 —Showing the surface areas of the back corresponding approximately to the 
areas of the spinal cord supplying the trunk and limbs. 



each area of skin is supplied by three nerve roots whose peripheral 
filaments overlap one another. 

For the ready study of the subject the cord has been separated 
into segments corresponding with the vertebrae covering it. The 
areas of anesthesia produced by spinal injury or disease are best 
described by Starr's well-known article and diagrams, from which 
we quote. In this connection the reader should refer to the tables 
on pages 82 and 83, showing the localization of the functions of the 
segments of the spinal cord. (See chapter on the Legs and Feet.) 



SENSATIOX IN THE SKIN 



177 



The anesthetic areas included in zones I and II in Fig 49 are due 
to a lesion involving the conus medullaris and the fourth and fifth 
sacral segments of the cord. These zones include the peritoneum, 
the posterior part of the scrotum in males, the vagina in females, 
and the mucous membrane of the rectum. Anesthesia in zone 
III is due to lesion of the third, fourth, and fifth sacral segments, 
and includes a large part of the buttock and the upper part of the 
thigh, posteriorly, in a triangular space. Zone IV is practically 
an enlargement of zone III in every direction, particularly toward 





Fig. 49. — Areas of anesthesia in lesions at various levels of the spinal cord from 

sacral V to lumbar II. (After Starr.) 

I. Sacral v. IV. Sacral t. 

II. Sacral iv. 1". Lnrabar v. 

III. Sacral in. VI. Lumbar in. 

VII. Lumbar n. 

the popliteal spaces, and is probably due to a lesion in the first and 
second sacral segments; but this needs confirmation by autopsy, 
as Starr points out. Zone V includes all the first four zones just 
named, and extends down through the popliteal space in a band- 
like shape; after it passes this space it descends the outer side of 
the leg and foot, sometimes ending at the ankle, sometimes at the 
sole or the three outer toes and half the next toe. Such an area 
indicates a lesion involving all the segments of the sacral cord, and 
extending into the lumbar cord to the fifth lumbar segment. Zone 
12 



178 



THE SKIN 



VI is caused by a lesion extending to the third lumbar segment, and 
when it is present the anesthesia covers the back of the thighs and 
legs and also the front of the thighs, except in an area which extends 
from above downward along the shin, sometimes to the foot, as in 
Fig. 49. If the foot is involved, the lesion in the lumbar cord is 
probably above the third lumbar segment. Zone VII, which is 
larger than all, follows a lesion in one of the four lumbar segments — 





Fig. 50.- 



AW 



-Areas of anesthesia Ironi lesions at various levels of the spinal cord from the 
second dorsal to the fifth cervical. (After Starr.) 



that is, all but the first. The line of anesthesia, Starr tells us, is 
lower in front than behind. When the abdominal wall is involved 
in the anesthesia the first lumbar segment is probably diseased. 

The area of the anesthesia from the level of the abdomen corre- 
sponds very closely to the levels in the cord if we allow for the 
space already mentioned, of two to three inches for the interlacing 
anastomosis of the nerve fibers of the posterior roots. 

They are about as follows, according to Thorburn: Wehn the 



SENSATJO.X J.\ THE SKIN 



170 



anesthesia is as high as the anterior inferior spine of the ilium, the 
lesion is at the twelfth dorsal vertebra; if at the umbilicus, at the 
eleventh and twelfth dorsal vertebrae; if up to the lowest floating 
rib, the whole eleventh dorsal vertebra; if from one to four inches 
above the umbilicus, the ninth and tenth dorsal, and perhaps part 
of the eighth dorsal vertebra; if as high as the nipples, the fourth 
dorsal vertebra; and if to the third rib, the lesion is as high as the 
second dorsal vertebra. 

Starr has also given us, in another paper than that already quoted, 
equally good ideas of the areas of anesthesia occurring above those 




Fig. 51. — Area of anesthesia from injury of the median nerve. Palmar surface. 



just described (Fig. 50). When the anesthesia extends to the 
arms and is found upon the inner side of the arm and forearm, 
reaching to the wrist, but not to the hand, and also involves a small 
zone on the extensor and flexor surfaces of the arm and forearm, 
the second dorsal region is the site of the lesion. If the anesthetic 
area includes the ulnar side of the hand, the palmar and dorsal sur- 
faces of the same, and the little finger, and extends in a narrow 
strip up to the axilla on both the anterior and posterior surfaces of 



180 



THE SKIN 



the arm and forearm, the lesion is probably at the level of the eighth 
cervical vertebra. When the zone involved extends to the middle 
of the central figure on the palmar and dorsal aspects, and runs up 
the centre of the forearm and arm, the seventh cervical area is dis- 
eased. Again, when the remaining skin of the hand up to the wrist 
and a narrow strip of skin up the forearm and arm on both surfaces 
to the axilla is affected, the lesion is at the sixth cervical vertebra, 
while anesthesia of the forearm and arm on the outer surface as 
high as the deltoid insertion indicate the fifth cervical vertebral area 




Fig. 52. — Area of anesthesia irom injury of the median nerve. Dorsal surface. 

in trouble. Lesions higher than this usually produce death before 
it is possible to test sensibility. 

Neuritis as a Cause of Anesthesia. — Anesthesia of the skin in any 
part of the body may be due not only to cerebral or spinal lesions, 
but also to neuritis or inflammation of the nerve trunk, or to some 
injury which impairs its functional activity by pressure, bruising, or 
cutting. As a rule, loss of sensation from neuritis occurs late in the 
disease, hyperesthesia of paresthesia being the earlier manifestations; 
but in some cases these are absent, and anesthesia begins at once. 



PLATE VI. 




Cervical Roots are represented by the letter C. Dorsal Roots by the letter D, 
and Lumbar Roots by the letter L. (Chart after Head.) 



SENSATION IN THE SKIS 



181 



The characteristic of such an anesthesia is that it is confined to 
the area supplied by the affected nerve, although the presence of a 
multiple neuritis may produce such a universal anesthesia by involv- 
ing all the nerves that this sign is masked. While a mono-anesthesia 
may be due to other causes, it is in the great majority of cases due to 
neuritis. The signs of an anesthesia due to neuritis are loss of motion 
and sensation, tenderness on pressure over the nerve trunks supplying 
the affected area, trophic changes in the tissues of the part, with the 
development of reactions of degeneration and pain in the involved 




Fig. 53. — Area of anesthesia in injury of the ulnar nerve. Dorsal surface. 



nerves or parts supplied by them. Somewhat similar symptoms 
occur in anterior poliomyelitis, but pain is not commonly present 
in this disease, and there is no anesthesia, either in children or adults. 
(See chapters on the Hands and Arms, and on the Feet and Legs.) 

Toxic peripheral neuritis producing anesthesia may arise from 
poisoning by arsenic, lead, alcohol, or mercury, from septic states of 
the body, and from the infectious diseases, particularly diphtheria, 
influenza, and typhoid fever. 

That due to the mineral poisons has in each case certain differen- 



182 



THE SKIN 



tial points of importance. The anesthesia of arsenical poisoning is 
more marked than in lead poisoning, in which condition it is often 
almost absent, and the lower extremities are very apt to be involved, 
whereas in lead poisoning, as is well known, the nerves of the arm 
are particularly susceptible. (See chapter on the Arms and Hands.) 
Arsenical neuritis may also produce pigmentation of the skin. In 
alcoholic neuritis the temperature of the anesthetic areas is often 
subnormal and there are nearly always mental disturbances repre- 
sented by delusions. In mercurial poisoning, shaking like paralysis 




Fig. 54. — Area of anesthesia from injury of the ulnar nerve. Palmar surface. 

agitans may be present. An analysis of the motor symptoms in 
all these cases is important, and the discovery of any one of these 
poisons in the urine, with the history of the patient, generally makes 
the diagnosis possible. 

Diphtheritic neuritis is quite common, and in 50 per cent, of the 
cases in which it occurs sensibility is lost or disturbed in the areas 
supplied by the involved nerves. 

Great care is needed in all cases of neuritis lest the mistake be 
made of diagnosticating the condition as one of locomotor ataxia, 
when in reality it is pseudotabes. 






SENSATION IN THE SKIN 



183 



It has already been stated that in neuritis the area of anesthesia 
is that supplied by the affected nerve. For this reason we can deter- 
mine what nerve trunk is affected by studying the area of anesthesia, 
always remembering, however, that the sensory fibers of the nerves, 
particularly in the hands and feet, anastomose so freely with those 
of adjacent nerves that the area of the anesthesia may not be exactly 





Fig. 55. — Cutaueous nerve supply of the trunk and upper extremity. (Fowler.) sa. Supra- 
clavicular nerve, iid. Second dorsal, ps. Posterior branches of the spinal nerves. Li. Lateral 
branches of the intercostal nerves, ai. Anterior branches of the intercostal nerves, c. Cir- 
cumflex nerve, ih. Intercostal humeral, w. Nerve of Wrisberg. i'cb. Internal cutaneous 
branch of musculospiral nerve, ecb. External cutaueous branch of musculospiral nerve. 
icb. Internal cutaneous nerve, mc. Musculocutaneous nerve, r. Radial nerve, u. Ulnar 
nerve, m. Median nerve. 



that supplied by the nerve involved; or, in other words, the presence 
of loss of power in a region supplied in health by a nerve which has 
been divided is constant, but very often sensation is not disturbed, 
even though the divided nerve be the sensory as well as the motor 
supply to the part. 

It is well to remember also that sensory disturbances of the skin 
following injuries of nerves are often not nearly so great as the 



184 



THE SKIN 



motor disturbance, even where there is no sensory transmission by 
anastomosis, and where they are present they usually disappear, 
more rapidly than the motor loss, as recovery takes place. 

The following facts are, therefore, of diagnostic interest. If the 
anesthesia is found to be due to a neuritis and to involve the palmar 
surface of the thumb, fore and middle fingers, the median nerve 



jc 




Fm. 56. — Cutaneous nerve supply of the lower extremity, n. Ilio-inguinal. iil. Second 
lumbar nerve, og. Genitocrural. ec. External cutaneous, mc. Middle cutaneous, ic. In- 
ternal cutaneous, is. Internal saphenous, ss. Small sciatic, ep. Branches from external 
popliteal, es. External saphenous, mcs. Musculocutaneous, pt. Branches of posterior tibial. 
(Modified from Gerrish.) 



is probably the one at fault (Figs. 51 and 52), and the area may 
even include in rare instances the backs of these fingers at their 
bases and the half of the third finger nearest the thumb. When 
there is disturbance of sensation in the ulnar side of the ring finger 



PLATE VII. 




Showing the Distribution of the Cranial Nerves, particularly the Fifth. 
(Modified from Arnold.) 

III. Branch of oculomotor to inferior oblique. V. The Gasserian ganglion, composed of the fibers 
of the sensory root of the nerve. (The plate would seem to indicate that the three branches of the nerve 
arise from this ganglion, but they do not, for the motor fibers do not enter the ganglion, but join the 
ensory fibers in the third branch, after they leave the ganglion.) XII. The hypoglossal nerve. 



SENSATION IN THE SKIN Is;, 

and in the skin of the little finger, there may be ulnar neuritis Figs. 
53 and 54). (See also chapter on the Hands.) The nerve supply of 
the skin of the entire upper extremity is well seen in Fig. 55. 

The development of sensory disturbances in the feet, resulting 
from neuritis, is as follows: When there is perverted sensation of 
the inner side of the foot from the tip of the big toe to the heel, 
and thence up the inside of the calf to the knee, the nerve involved 
is the long or internal saphenous. When the dorsal surface of the 
foot has its cutaneous sense disturbed the nerve involved is the 
musculocutaneous, a branch of the external popliteal. Disturbance 
of sensation on the outer side of the foot and calf indicates failure 
of function in the external saphenous, which is composed of the 
cutaneous branches of the external and internal popliteal nerves. 
Disturbed sensation on the posterior surface of the calf also indicates 
trouble in the external saphenous nerve and communicans peronei, 
while when the sensation of the skin of the heel is disturbed the 
plantar cutaneous nerve, a branch of the posterior tibial, is involved 
(Fig. 56). 

In the skin of the thigh the anterior surface is supplied by the 
middle cutaneous nerve, which is a branch of the anterior crural; 
on the inner side by the internal cutaneous, also a branch of the 
anterior crural; and on the outer side by the external cutaneous, 
which arises from the second and third lumbar nerves. Laterally 
the external cutaneous gives the supply. Posteriorly the small 
sciatic gives the nerve supply to the skin. 

Anesthesia of the greater portion of the skin of the thigh, except 
in a narrow strip on the back part and in the area supplied by the 
internal saphenous nerve, often occurs as the result of paralysis of 
the anterior crural nerve, arising from pelvic tumors, psoas abs< 
and vertebral disease. 

Facial Anesthesia and its diagnostic meaning are still to be con- 
sidered. W T hen it occurs it indicates that the fifth nerve, or its 
nucleus, is involved. 

If the area be that of the forehead, the upper eyelid, the conjunc- 
tiva, and the nostril, the ophthalmic branch of the fifth nerve is at 
fault, and the lesion is probably at the sphenoidal fissure or within 
the orbit, and reflex winking of the eye no longer takes place because 
the conjunctiva is anesthetic. 

If the skin of the upper part of the face is anesthetic, the superior 
maxillary branch is involved; and if the skin of the temporal region 
and that of the jaw and the under lip are anesthetic, the inferior 
maxillary branch is diseased. When both of these branches are 
paralyzed there is probably a tumor of the superior maxillary bone; 
and if the entire area of the three branches is anesthetic, the Gas- 
serian ganglion may be the part affected, and this will be accom- 



186 THE SKIN 

panied by trophic changes in the anesthetic parts. The most com- 
mon cause of anesthesia of the trifacial is, however, neuritis. 
Romberg makes the following differential statement : 

(a) The more the anesthesia is confined to single filaments of the 
trigeminus, the more peripheral the seat of the cause will be found 
to be. 

(b) If the loss of sensation affects a portion of the facial surface, 
together with the corresponding faucial membrane, the disease may 
be assumed to involve the sensory fibers of the fifth pair before they 
separate to be distributed to their respective destinations; in other 
words, a main division must be affected before or after its passage 
through the cranium. 

(c) When the entire sensory tract of the fifth nerve has lost its 
power, and there are at the same time derangements of the nutritive 
functions in the affected parts, the Gasserian ganglion, or the nerve 
in its immediate vicinity, is the seat of the disease. 

(d) If the anesthesia of the fifth nerve is complicated with disturbed 
functions of adjacent cerebral nerves, it may be assumed that the 
cause is seated at the base of the brain. 

Other Disturbances of Sensation than Anesthesia. — The other dis- 
turbances of sensation of the skin than anesthesia, which are usually 
subjective rather than objective, are paresthesia, hyperesthesia, 
and analgesia. 

Paresthesia — numbness, tingling, or burning — is seen in nearly 
all cases in which anesthesia ultimately develops as a result of 
organic lesions. When a patient complains that he cannot feel the 
contact of clothing about his feet and legs, or that the feet when he 
walks feel as if wrapped in some thick material, or as if he were 
walking on moss, or that the soles of his feet feel as if they were 
numb and at the same time tickled by ants walking over them, the 
characteristic sensory disturbance of the skin seen in locomotor 
ataxia is present. 

Often there is tingling or numbness of the fingers, particularly of 
the ring and little fingers, and a sensation as if a girdle were about 
the patient is common. These are the subjective disturbances of 
sensation in tabes dorsalis, and, as they are often the earliest mani- 
festations of the disease, possess great diagnostic importance. The 
objective sensory perversions consist in the discovery by the physi- 
cian, when studying the sensibility of the skin, of areas of anesthesia, 
analgesia, and hyperesthesia which are usually bilateral. Belmont 
has stated that we also find these areas in spinal syphilis, either 
on one or both sides. Numbness, tingling, and formications affect- 
ing the skin are also often early symptoms of brain tumor in the 
area supplying the affected part, and this possibility is increased 
if there is associated spasm. The actual objective sensibility of the 



SENSATION IN THE SKIS \\~ 

skin may be preserved for some time after these symptoms appear, 
or it may be impaired almost at the outset, owing to the involvement 

of all or part of the sensory tracts in the cord. Similar symptoms 
are often seen in the early stages of myelitis. They are very fre- 
quently seen after injuries to nerves, and severe tingling in its acute 
variety occurs when the "funny bone" of the elbow is knocked 
against an object, owing to bruising the nerve. It is also seen in 
cases of aconite poisoning, and when the hands have been exposed 
to carbolic acid. Paresthesias are also frequently seen in eases of 
neurasthenia. 

Perversions of sensation in the skin sometimes take a curious 
form, as, for example, that known as allochiria, in which a sensory 
impulse in one hand is referred by the patient to the opposite hand. 
This is seen in tabes dorsalis, myelitis, multiple sclerosis, and hys- 
teria. In other cases, as in paralysis agitans, this perversion takes 
place in the form of failure to distinguish heat and cold, and subjec- 
tive sensations of extreme heat are felt. The part affected may 
actually have its temperature raised several degrees. 

Magnan asserts that a sensation as if a worm or bug were crawling 
under the skin is indicative of cocaine intoxication. 

Very closely associated with the numbness of hysteria or neuras- 
thenia, and lying between functional and organic disease of the 
nerves, is that condition called a ro paresthesia or waking numb- 
ness. This state is usually seen in women past middle life, but 
may occur in men. On waking in the morning marked formication 
and numbness of the fingers are present, which usually pass off as 
the day progresses, but as the condition becomes more marked they 
may last all day. While there is no anesthesia, strictly speaking, 
the disturbed sense of touch renders sewing or performing any 
small act with the fingers almost impossible. These sensations may 
be confined to the area of one nerve, as the ulnar, or involve all the 
skin of the hands, or more rarely of the feet. General nervous 
excitability is usually associated with the local manifestations. 
Sometimes the scalp may be the area involved. 

Acroparesthesia is to be separated from the sensory disturbances 
of hysteria by its irregular outline, for generally in the latter disease 
the areas are distinctly outlined, by the fact that the hysterical 
condition is usually unilateral, and by the absence of the charac- 
teristic general hysterical symptoms. From organic disease it is 
separated by the absence of the signs of neuritis about to be described. 
and by the absence of tenderness, pain, and loss of power. From 
cerebral or spinal disease it is separated by the absence of symptoms 
produced by lesions in these parts, and by the facts that in both 
these lesions there is paralysis of motion in association with the 
sensory disturbance, and in the case of spinal lesions the symptoms 



188 THE SKIN 



are usually in the legs ; while acroparesthesia generally manifests 
itself in the hands. 

Closely associated with paresthesia, if not an actual form of it, 
is the "girdle sensation;" that is, the patient feels as if a tight belt 
were strapped around a limb or the trunk. This is seen as a promi- 
nent symptom in locomotor ataxia, myelitis, and tumors of the cord 
or its envelopes. When the lesion is in the lower cervical or dorsal 
region the sensation is in the chest or abdomen; but this relationship 
between the growth and the sensation of constriction is not always 
constant. (See chapter on the Feet and Legs.) 

Hyperesthesia of the skin is an important symptom of both 
hysteria and neurasthenia, and its discovery in association with the 
peculiar symptoms which occur in the former morbid state confirm 
a diagnosis most positively. The most important and curious of 
these hyperesthesias are the so-called hysterogenous zones, or, in 
other words, areas involving the skin and subcutaneous parts, which 
possess great sensitiveness, and which, when pressed upon, cause in 
many cases convulsive seizures of the hysterical type. Not only is 
this true, but in addition it is a noteworthy fact that after the nervous 
disturbance produced by this means is set in motion, a second 
pressure on the hysterogenous zone may arrest the seizure. These 
zones commonly exist over the ovaries, in the groin, about the 
periphery of the mammary glands, or upon the spine in the lumbar 
or dorsal region. (See chapter on Pain.) 

The hyperesthesia due to neurasthenia is to a great extent spinal 
in character, but the skin of the rest of the back, particularly over 
the great muscles on each side of the spine, may also be involved. 
Often the neurasthenic patient or one who has phosphaturia will 
complain that in brushing or combing the hair pain or extreme sen- 
sitiveness is developed upon the scalp, and there may be tender 
areas on the chest. These areas in neurasthenics can hardly be 
confused, even by the careless, with the hyperesthetic zones of 
hysteria, and the personal history and characteristics of the indi- 
vidual aid still further in separating the two conditions. 

Hyperesthesia of the skin, aside from that seen in hysteria and 
neurasthenia, occurs in peripheral neuritis and locomotor ataxia, the 
skin of the back being particularly tender in the latter disease, and 
the excessive sensitiveness is frequently seen in a zone extending a 
little above the anesthetic areas of transverse myelitis, this hyper- 
esthetic area being soon rendered anesthetic by the progress of the 
disease. Hyperesthesia in the skin of the limbs is also rarely seen 
in myelitis, and when there is motor paralysis of one side and sen- 
sory paralysis of the other it is commonly found on the side on 
which motion is lost. A condition of excessive dermal hyperesthesia 
is also present in cerebrospinal meningitis, in which disease it is 



SENSATION IN THE SKIN 189 

often a very early symptom. It usually appears first in the legs, 
then in the hands and arms, and, finally, the skin of the face and 
head become involved. 

Hyperesthesia of the skin occurs, often associated with skin 
eruptions, in that very rare condition called chronic leptomeningitis. 

Motor symptoms are nearly always present if the cord becomes 
involved. 

Hyperesthesia of the skin is considered by some authors to be, 
when found in association with other characteristic symptoms, 
almost pathognomonic of brain tumor. It may be found on the 
scalp, over a large part of the body, or in the part which is paralyzed. 
It is also found during the convalescence of typhoid fever and in 
relapsing fever. It also appears in the paralyzed side of persons 
suffering from hemiplegia, in the area supplied by a nerve suffer- 
ing from neuralgia, particularly that of a migraine type, in the scalp 
of persons suffering from gout, and in the same area in women about 
the time of the menopause. 

General tenderness of the skin or deeper tissues is quite frequently 
seen in cases of rickets and scurvy, the child crying whenever it is 
moved, as if sore and tender, and tender spots often appear over the 
ribs in cases of pleurisy. 

Sometimes in a neurotic girl about the time of puberty, or in a 
woman, one breast becomes exceedingly painful and tender, and 
the skin of the breast becomes so hyperesthetic that the slightest 
touch causes pain. The whole breast is, moreover, tender, and 
movement of the arm may be impossible, owing to pain thereby 
caused in the gland. This hysterical breast can be separated from 
the painful breast due to a tumor by the general diffuse character 
of the swelling, the failure to outline any distinct mass, the neurotic 
character of the patient and her age. 

The hyperesthesia of chronic alcoholism may be both dermal and 
deep, and is well marked along the course of the peripheral nerves, 
particularly where they emerge from deeper structures. It is also 
seen in the neuritis of lead and arsenical poisoning. 

Increased sensibility of the skin may follow the use of opium or 
ergot, and is met with in the course of, or as a sequel of, influenza, 
and in some cases of profound anemia. 

In some cases hyperesthesia is an early sign of the onset of non- 
tuberculous leprosy, and will generally be found in the course of 
the ulnar or sciatic nerves in such cases. 

A very interesting fact from a physiological and diagnostic point 
of view is that disease of the internal organs or viscera often pro- 
duces areas of hyperesthesia or tenderness upon the skin, which 
may in future be used to aid in the localization of the lesions. This 
subject has been well studied by Head (Brain, 1893 and 1894), 



190 THE SKIN 

from whose researches much information may be derived, but the 
results of which will have to be confirmed in many cases before 
they can be used as diagnostic guides. (See article on Pain.) 

Pain in the skin is very various in its manifestations, and nearly 
always is due to functional nervous troubles. Duhring has noted 
a boring sensation in some cases. It should direct the physician's 
attention to the possibility of hysteria or tabes dorsalis. 

Pruritus, or intense itching of the skin, may be due to contact 
with some irritant, but its presence, if persistent, particularly if 
widespread or near the genitals, should always raise a suspicion of 
diabetes mellitus, or chronic lead poisoning, or gout, or chronic con- 
tracted kidney. Very rarely opium may produce a pruritus, and 
jaundice is nearly always accompanied by some itching. Pruritus 
about the anus is often due to piles, gout, and diabetes. 

Finally, one important point is to be remembered, viz., we cannot 
attempt to make a general diagnosis merely from a study of the 
areas of anesthesia or other perverted sensibility of the skin in any 
case. The results obtained from studies of the sensation of the 
skin are only to be used as additions to the motor and other 
symptoms which will be found discussed under the chapters on 
the limbs 



CHAPTER VII. 

THE THORAX AND ITS VISCERA. 

The inspection of the normal and abnormal chest — Their topography — Altera- 
tions in the shape of the thorax — The rhythm of the respirations— The 

results of using inspection, palpation, percussion, and auscultation in 
health and disease — The characteristic signs and symptoms of the various 
diseases of the thoracic organs. 

The chief contents of the thoracic cavity consist of vital organs, 
which are, unfortunately, only too often subject to disease. A care- 
ful study of the signs associated with the normal functions of these 
parts is, therefore, of importance, as is also that of the symptoms 
indicating pathological changes. While it is true that in many 
instances patients present themselves to the physician with well- 
marked objective and subjective symptoms pointing to abnormalities 
in the organs of the chest, it is also a fact that in many others none 
of these signs exist, or they exist in such an indefinite manner that 
the physician's attention is not attracted to them, and as a result im- 
portant thoracic changes from the normal are overlooked or made 
light of. We base our diagnosis of the character of a case on the 
changes which we find in the thorax as to its contour and as to its 
movements, on the respiratory and cardiac sounds, and on the other 
physical signs about to be described. 

The measures used in the physical diagnosis of the diseases of 
the thoracic organs are Inspection, Palpation, Mensuration, Percus- 
sion, and Auscultation. 

INSPECTION. 

Before we proceed to the study of the alterations produced by 
disease in this portion of the body, we must have a clear conception 
of the appearance of the chest in health. 

Inspection of the normal chest when free from clothing will 
reveal the fact that it is conical in form, the broader part of the cone 
being in the upper portion. Above the clavicles there is usually a 
slight depression (the supraclavicular fossa), and below the clavicles, 
which may be somewhat prominent, there is a slight convexity which 
extends as far down as the fourth rib. This convexity varies con- 
siderably according to the muscular development of the individual, 
the formation of the bony portion of the chest wall, and the deposit 



192 



THE THORAX AND ITS VISCERA 



of fat in the subcutaneous tissues of the chest. The nipple is by no 
means as definite a landmark as is sometimes thought, as its position, 
in respect to the ribs under it, varies greatly in different individuals; 
and it is still further altered in its position by the presence of much 
fat under it, or, again, in multiparous women by the relaxation 
of the breast. In the average adult male or virgin female the 




Fig. 57. — The regions of the anterior aspect of the chest. The vertical lines are called the 
mammillary lines. The upper squares form the superior thoracic area; lower squares form the 
inferior thoracic area, and the lowest square the epigastric. 

nipple is on a level with the fourth rib or fourth interspace. The 
ribs in a well-developed person are not prominent in the upper two- 
thirds of the chest, but in the lower third are more readily seen, 
particularly at the sides, because of their thin covering by muscles 
and the subcutaneous tissues and the skin. The sternum in front 
and the spine behind are normally in the middle line. Over the 
top of the sternum is a depression called the episternal notch. 



INSPECTION 



193 



The result of lateral examination of the normal chest when com- 
pared with the front view will show that the anteroposterior diam- 
eter is less than the lateral diameter. 

The surface of the ehest anteriorly, posteriorly, and laterally has 
been arbitrarily divided by imaginary lines into spaces, as shown in 
the accompanying figure (Fig. 57). The lines running from the 
middle of the clavicles downward through the nipple are called 
the mammillary lines. The parasternal line, not shown in the 
figure, is a vertical line half-way between the middle of the sternum 
and the mammillary line; and a line running down the side from 




Fig. 58. — Position of heart in relation to ribs and sternum. (Tyson.) 



the axilla is called the midaxillary line. These artificial divisions 
enable us to describe the locality of signs and symptoms. 

If we could see through the chest wall, we would find that the 
lungs, extend above the clavicles. Immediately back of the inner 
end of the left clavicle is the beginning of the innominate vein, and 
back of this, again, the common carotid artery. On the right side 
the innominate artery bifurcates just behind the junction of the 
sternum and clavicle. The figure above shows the relation of 
the cavities of the heart and its great vessels to the chest wall 
(Fig. 58). 

Anteriorly the lung extends downward as far as the sixth rib on the 
13 



194 



THE THORAX AND ITS VISCERA 



right, but the dome of the liver reaches to the level of the fourth 
interspace. On the left side the lung extends a little lower than on 
the right side. Laterally the lung on both sides extends to the ninth 
rib in the midaxillary line. Posteriorly on the right side the lung 
extends as low as the tenth rib, and on the left side as low as the 
ninth. 

Marked variations in the shape of the chest occur in healthy 
individuals without possessing any direct pathological significance. 
Thus, it is very common to see one shoulder slightly higher than 
the other, and, in the case of clerks or persons who work much at 





Fig. 59. — The alar chest of phthisis. 



Fig. 60. — Side view of same patient. 



a desk, the left shoulder is very apt to be somewhat elevated. Occu- 
pations which cause the individual to assume certain positions, or to 
use certain muscles continually, also cause variations in the contour 
of the thorax. 

Inspection of the Abnormal Chest. — The configurations of the 
chest which show a tendency to disease or the results of attacks 
of disease are numerous. 

The most familiar of these is the so-called phthisical chest, which 
has been called the "alar chest," because the scapulse stand out 
from the back like wings (Fig 59). The anteroposterior diam- 
eter, particularly in the upper two-thirds, is very slight, and instead 



INSPECTION 



195 



of convexity of the anterior surface there may be flattening or hol- 
lowness (Fig 60). This area scarcely moves on inspiration, but 
the lower third, which is bulging, moves markedly with the respi- 
ratory efforts, as does also the epigastrium. The shoulders are very 
sloping; the neck, anteriorly, recedes at the episternal notch, but 
springs forward toward the Adam's apple and the chin. The ribs in 
the phthisical chest fall downward toward the belly from their points 
of origin, instead of coming forward in a normal curve (Fig. 61). 

If, on the other hand, the chest bulges anteriorly and posteriorly 
to such an extent that the anteroposterior diameter is greater than, 




Fig. 01. — Phthisical chest. 



or equal to, the lateral diameter, and if this bulging is fairly uni- 
form, the shoulders being elevated, the back rounded, and the neck 
short in appearance from the raised shoulders, the patient is prob- 
ably a sufferer from emphysema of the lungs. This chest is often 
called the "barrel-shaped chest." (See Fig. 63.) The chest wall 
moves very little or not at all with the respiratory movements, which 
are chiefly diaphragmatic. 

Bulging of the chest wall results, in its most diffused type, from 
the presence of chronic pleural effusion and pneumothorax; bulging 
of a limited area also arises from cardiac hypertrophy, particularly 



190 



THE THORAX AND ITS VISCERA 



that occurring in childhood; from aortic aneurysm, causing bulging 
by pressure (Figs. 82 and 83) ; from pericardial effusion; and, finally, 




Fig. 63. — Emphysema of the lungs. 
Shows barrel-shaped chest. 



Fig. 64. — Bulging of the chest wall, with erosion 
of ribs, from aortic and innominate aneurysm. 



INSPECTION 



107 




198 



THE THORAX AND ITS -VISCERA 



from mediastinal growths. Marked bulging over the lower part of 
the chest on the right side should cause us to look for some hepatic 
affection, as well as to examine for pleural effusion, and, if the bulg- 
ing is low down on the left side, to examine for pleural effusion or 
enlargement of the spleen. 

Bulging or protrusion of the sternum and the cartilaginous por- 
tions of the ribs attached to it is called "pigeon breast," and is 
due either to rickets or to the presence of some obstruction to respi- 
ration of a more or less chronic character during the time the chest 




Fibs. 66 and 67. — Showing shrinkage and partial collapse of left side of chest and distortion 
of spinal column due to chronic tuberculous pleurisy in a boy of fifteen years. (From the 
author's wards in the Jefferson Medical College Hospital.) 

wall was soft and capable of being moulded. Sometimes on each 
side of the sternum, over the costal cartilages, there is seen a groove 
or depression as the result of rickets. In other cases a depression 
or groove extends from the ensiform cartilage backward on either 
side toward the spine. This is called " Harrison's groove." and is 
developed in children with poor bony systems, as the result of 
repeated attacks of asthma or other obstructive respiratory difficulty. 
When examining the chests of children the physician will often 
notice swellings of the tissues at the costocartilaginous junctions, 
which look and feel to the touch like large beads under the skin. 



INSPECTION 



199 



These beaded ribs arc indicative of rickets, and arc a manifestation 
of the general tendency to epiphyseal enlargement. This beading 
is usually most marked on the lower ribs (Fig. 65). 

Finally, unilateral bulging of the chest may be due to curvature 
of the spine, which part of the body should always be examined 
before a diagnosis as to deformity of the chest is attempted. 

Shrinkage of the chest in one part may be due to the contraction 
of old pleural adhesions (Figs. Go and 07). It is sometimes seen 






Fig. 68. 



A case of empyema of the right side, showiDg obliteration of the intercostal spaces 
and hypertrophy of the mammary gland. (From the author's wards.) 



over the diseased area in pulmonary tuberculosis, and may be appa- 
rently present, but in reality due to wasting of the tissues covering 
the part. 

Marked enlargement of the mammary gland on the affected side 
is sometimes seen in pulmonarv tuberculosis, particularlv in males 
(Fig. 68). 

The shape and surface of the chest having been studied, we can 
go farther and learn much from its movements in respiration: first, 
from the rapidity of respiration; second, from the respiratory rhythm; 



200 • THE THORAX AND ITS VISCERA 

third, from the character of the breathing; and, fourth, from the 
movements of the ribs. 

When counting the respirations the physician should always 
endeavor to do so without letting the patient know what he is doing, 
since it is difficult for many persons not to control their breathing 
when their attention is called to it. Generally the eye can detect 
the frequency of the breathing by simply watching the movement 
of the chest, or the information can be gained by resting the hand 
on the abdomen or thorax, while the wrist is also held and the doctor 
is apparently taking the pulse. In the newly born child in perfect 
health the respirations are often as high as 44, but in the adult 
male at rest they are usually about 14 to 16 per minute. During 
sleep the number may fall to 8 or 10. The ratio of pulse to 
respiration is usually 4 to 1, but in rare instances in disease it may 
be 1 to 1. 

Rapid respira'ions not due to any recent sudden exertion are 
nearly always indicative of respiratory trouble, primary or second- 
ary. If the primary trouble be in the lung, it will probably be 
due to croupous pneumonia, catarrhal pneumonia, severe bronchitis, 
asthma, tuberculosis, pulmonary abscess, or tumors of the lungs. 
If it be due to secondary lesions in the lung, it may rise from pul- 
monary edema due to nephritis, from congestion or hypostatic 
exudation as the result of a weak heart, from pulmonary embolism, 
from a pleural effusion which seriously interferes with the action of 
the lung or lungs, from growths in the mediastinum pressing upon 
bloodvessels and so causing exudation into the lungs or pleura, and 
from ascites or abdominal growths pressing upon the diaphragm. 
Usually in these states the respirations will be not only more rapid 
than normal, but difficult or labored. Sometimes in hysterical 
rapid breathing the respirations reach 150 per minute. This is 
not voluntary, and the diaphragm moves very little, the chief breath- 
ing being costal. If the lungs be clear of trouble, then the difficulty 
may be present in the trachea or larynx, either as the result of spas- 
modic contraction of these passages or because they are occluded by 
growths, such as papilloma or malignant growth, inside or outside, 
or aneurysm which may act by pressure, thereby narrowing the 
tube. Any agency which interferes with the proper oxygenation 
of the blood causes rapid breathing unless at the same time the 
respiratory centre is depressed. 

There are, moreover, several other causes which affect the char- 
acter of the respiration without affecting the larynx or lung tissues 
directly or indirectly. These are fever, which acts as a respiratory 
stimulant, and excitement, nervous or mental, particularly that of 
hysterical patients. Again, apoplectic seizures, uremia, and diabetic 
coma may be accompanied by rapid breathing. 



INSPECTION 201 

The respirations are slowed or decreased in number by great 
obstruction to the entrance of air into the lungs from any cause, so 
that it is difficult to inhale the air, by the action of poisons made 
in the body, as the poisons of uremia and diabetes; by the effect of 
poisons swallowed or absorbed in other ways, notably opium, chloral, 
aconite, chloroform, or antimony. 

The rhythm or relative time of inspiration, expiration, and the 
pause is in health in the mouth and trachea as follows: If 10 repre- 
sents a complete respiratory cycle, inspiration is represented by ">, 
expiration by 4, and the pause by 1. If it is difficult for air to enter 
the chest, as in spasmodic croup, the inspiration is much prolonged. 
This prolongation is also sometimes very marked in cases of par- 
alysis of the posterior crico-arytenoid muscles. If there is difficulty 
in expelling the air, the expiration is prolonged, as in asthma and 
in emphysema. 

The most remarkable change in rhythm is the so-called Cheyne- 
Stokes breathing, in which the patient after a pause of several sec- 
onds begins to breathe with gradually increasing rapidity and depth, 
and then, after reaching an acme of hurried respirations, gradually 
decreases their rapidity and depth until they fade to nothing, when. 
after a pause, the same process is repeated. This breathing is seen 
commonly in apoplexy, in uremia, in brain tumor, in cerebrospinal 
fever, in meningeal tuberculosis, in some rare cases of cardiac val- 
vular disease, probably as the result of embolism, and in hematuric 
malarial fever. Rarely it occurs in cases of acute febrile disease, 
as typhoid fever, scarlet fever, pneumonia, whooping-cough, and 
puerperal septicemia. It may also be met with in the course of 
diabetes. Its presence is an exceedingly bad prognostic sign, but 
cases of recovery after its onset have been observed, and Murri has 
reported a case in which Cheyne-Stokes breathing lasted forty days, 
and Sansom one in which it lasted 108 days. If the cause be an 
acute disease, recovery is more common after this symptom than 
if it be due to some chronic process with an acute exacerbation. 

Labored breathing (dyspnea) is seen in all cases in which the 
blood cannot be provided with sufficient oxygen owing to obstruc- 
tion to the entrance of air into the chest, to spasm of the bronchioles, 
or to the occluding of the air vesicles by any form of exudate, croup- 
ous, catarrhal, or serous. These conditions may be primary or 
secondary to disease elsewhere, as in uremia or cardiac disease. 
Inspection of the chest in such a case shows great activity of the 
accessory respiratory muscles, such as the sternomastoid, the scaleni, 
the pectorals, and the abdominal recti. The nostrils are dilated 
and the face is anxious. The posture of the patient is that of sitting 
up in bed. 

Sometimes when the chest is flexible, as is that of a child, the 



202 THE THORAX AND ITS VISCERA 

inspiration is jerking when there is obstruction to breathing. This 
is due to the fact that the chest is forced into expansion by muscular 
effort, and at the same time is subjected to the external atmospheric 
pressure, while the air enters the lung slowly and irregularly owing 
to the obstruction. 

The function of breathing and the movements of the chest are 
closely associated. In men the respiratory movements chiefly affect 
the lower ribs and the abdominal walls, owing to the fact that as 
the diaphragm descends it pushes the abdominal contents downward, 
so causing abdominal bulging. In women, however, this is not so 
marked, and the breathing is chiefly costal, the upper part of the 
chest moving more than the lower (costal breathing). If abaomi- 
nal breathing is absent in a man and is replaced by breathing of the 
costal type, we can be assured that the movements of the diaphragm 
are impaired by the pressure of fluid in the abdomen (ascites);. 
by peritonitis, causing fixation of the diaphragm, owing to pain; by 
the presence of large growths in the abdomen, or by great enlarge- 
ment of the liver and spleen. Other possible causes would be a 
subphrenic abscess or a greatly enlarged cystic kidney, or hydro- 
nephrosis. 

If the costal breathing of a woman is absent, there is nearly 
always some pulmonary cause for it, such as faulty development, 
or, if due to disease, its absence arises most commonly from tuber- 
culosis or pleurisy, or old pleural adhesions which bind down the 
chest wall. 

In this connection should be mentioned the "wavy breathing" 
met with most commonly in pneumonia, a condition in which inspira- 
tion and expiration do not seem to occur regularly or evenly all over 
the chest, one part filling or emptying a moment before the other. 
This usually indicates a grave pulmonary condition. 

It is also necessary to notice the extent of the chest movements. 
These are very limited in the characteristic chest of a person having 
a tendency to tuberculosis, and in the barrel-shaped and rigid chest 
of emphysema of the lungs. Deficient respiratory movement is 
not only a predisposing cause of lung disease, but an important 
diagnostic sign. When one side of the chest moves more than the 
other to a considerable extent, we suspect, in the side which moves 
slightly, a pneumonia, a pleuritis, a pleuritic effusion or adhesion, 
tuberculous consolidation or fibroid lung, provided that the patient 
has not naturally a greater development on one side than the other, 
or has not pursued a trade or occupation causing unilateral hyper- 
trophy. 

While inspecting the surface of the chest the physician should 
also note the presence or absence of enlarged or pulsating blood- 
vessels on its surface or about the base of the neck. The cervical 



PLATE VIII 




A frozen section made in a plane lying 5 cm. in a posterolateral direction from the nipples and too 
Hear the anterior surface to show the large vessels of the chest and neck. The patient died of acute 
left-sided pneumothorax, resulting from tuberculosis. The section reveals the collapsed left lung, the 
lir space about it, the heart pushed far to the right in its sac, and the anterior border of the right lung 
compressed by the heart. The right lung is also greatly displaced, and the air has pushed the diaphragm 
downward on the left side. (Ponfick.) 



INSPECTION 203 

vessels arc commonly seen to be distended in cases of advanced 
emphysema of the lungs and in chronic bronchitis. Systolic pulsa- 
tion of the jugular veins indicates tricuspid regurgitation. Again, 
in eases of thoracic aneurysm pressing upon the superior vena cava 

and innominate veins we find spongy venous masses above the clavi- 
cles, and the veins of the trunk and arms may be engaged. Intra- 
thoracic growths produce similar symptoms. 1 Pulsation in the 
cervical vessels is also sometimes seen in cases of -even- anemia 
and in eases of aortic dilatation with regurgitation. 

Sometimes when a patient is placed flat on his back with his feet 
pointing straight toward a window (cross-lights being excluded | and 
the chest exposed, the following phenomenon can be observed during 
forced respiration: along both axillae a sort of shadow is seen to 
descend during deep inspiration from about the seventh to about the 
ninth ribs, passing up again during expiration. It is best seen in 
spare, muscular young persons of either sex. The observer should 
stand with his back to the light. It is called Litten's sign. 

This phenomenon is nearly or entirely absent in the following 
conditions: (1) Fluid or air in the pleural cavity. (2 | Obliteration 
of the pleural cavity by adhesions. (3) Advanced emphysema of 
the lungs. (4) Pneumonias of the lower lobe. 5) Intrathoracic 
tumors low down in the chest. 

Slight and limited pulsations on the chest wall elsewhere than 
over the apex beat may be due to many causes. 2 See Palpation. 
When they are seen in the second or third interspace on the right 
side they are due as a rule to displacement of the heart, which has 
been drawn to the right by mediastinopericarditis or contraction of 
the right lung and pleura as a result of chronic disease. If the pulia- 
tion is lower than this, it is usually due to a dilated right auricle, or 
displacement of the entire heart, as in a left-sided hydro-, pneumo-, 
or pyothorax. (See Plate YIII.) If the pulsation be on the left 
side of the sternum, then it may arise from a displaced apex beat due 
to effusion, or to retraction of the pleura which has become adherent 
to the pericardium, or fibrosis of the lung may be the cause. Finally, 
there may be marked epigastric pulsation. This is due to dis- 
placement of the heart by left-sided pleural effusion, which pushes 
the heart to the right and downward, to hypertrophy of the right 
ventricle, to pulmonary emphysema, often a cause of enlargement 
of the right side of the heart, and, finally, it may be due to trans- 
mitted pulsation of the abdominal aorta. If the latter is the cause, 
it can usually be determined by deep palpation that the pulsation 
arises from this vessel. Rarely it is due to the transmission of the 

1 See "The Pathology, Clinical History, and Diaguosis of Diseases of the Mediastinum."' by 
the author. Fothergillian Prize Essay of Medical Society of London for 1 888. 

- These are spokeu of here because they can often be seen yet cannot be felt with the 
finger tips. 



204 THE THORAX AND ITS VISCERA 

aortic impulse by a tumor which overlies the artery. If this is the 
case, it will be found that when the patient takes the knee-chest 
posture the pulsation disappears because the growth falls awa) 
from the bloodvessel. 

If the epigastric pulsation is in the nature of a systolic retraction, 
then it is probably due to indurative mediastinopericarditis. 

Rarely, on inspection of the chest anteriorly, a curious retraction 
of the interspaces near the level of the apex beat is noticed to occur 
with each systole of the heart. This is usually indicative of an 
adherent pericardium, and when on inspection of the posterior 
surface of the chest such retraction is seen at the level of the eleventh 
interspace it is called "Broadbent's sign" of adherent pericardium. 
This movement is supposed to be due to the heart pulling on the 
central tendon and muscular portion of the diaphragm. 

(For the further discussion of the significance and position of 
cardiac pulsations and thrills, see Palpation below.) 



PALPATION. 

Palpation of the chest is usually performed by placing the finger 
tips or the whole hand, palm downward, on the chest. This method 
reveals alterations in its contour and in its elasticity. It will also 
reveal the ability of the thoracic viscera and the chest wall to trans- 
mit vibrations produced by the voice (vocal fremitus). This so- 
called vocal fremitus depends upon the fact that below the vocal 
bands lies a column of air which reaches to the vesicular portions 
of the lung, and when an individual speaks this column of air is 
put into vibration, and these vibrations are in turn transmitted to 
the chest wall. Of course, a chest wall greatly thickened by fat or 
by highly developed muscles will not transmit these vibrations as 
readily as a thin chest wall; but aside from these causes of varia- 
tions in fremitus in health we have a number of causes in disease 
which greatly modify vocal fremitus. It must be remembered, too, 
that this vibration is more marked in men than in women and chil- 
dren, because the voice of a man is so much louder and has greater 
volume. Vocal fremitus is also greater on the right side than on 
the left, because the principal bronchus supplying this lung is larger 
than that of the left side, is joined to the trachea at a less acute 
angle, and is nearer the vertebral column; and, again, as recently 
emphasized by Cary, the bronchus going to the right upper lobe is 
given off at a point very near the origin of the right bronchus, and 
in many cases " fully two and a half inches above the correspond- 
ing left bronchial tube." Sometimes this upper tube comes off the 
trachea directly. 



PALPATIO \ 



205 



Palpation of the Abnormal Chest. — The conditions of the lung 
which cause a decrease in vocal fremitus are pleural effusions of any 
kind, which not only cut off the transmission of sound, but by their 
contact prevent vibration of the chest wall; pneumothorax, which 
causes collapse of the transmitting medium, the lung; any condition 
which causes occlusion of a large bronchus, such as a tumor or a 
large mass of mucus, and great pleural thickening. When the vocal 
fremitus is increased it is an indication of pneumonia, of tuberculoid 
thickening or consolidation of the lung, of the presence of a cavity 
or of tumor in the thorax touching the chest wall. Fremitus is 
increased in these conditions because the consolidated lung trans- 
mits the vibrations of the air in the bronchial tubes to the chest 




Fig. 69. — Area of normal apex beat. 



wall, or, in the case of a cavity, the sound is transmitted directly 
to it, and it there causes so great a vibration of the air in the hollow 
space that the vibration of the chest wall is marked. (In this con- 
nection, see part of this chapter on Auscultation.) 

Palpation of the chest wall will also give information as to the 
position and character of the cardiac pulsations. Thus, the apex 
beat of the heart in persons standing erect will usually be felt, in 
those who are not inordinately fat and who are healthy, between 
the fifth and sixth ribs, about two inches to the left of the sternum 
(Fig. 69). If the apex beat is below this level, its depression may be 
due to enlargement of the heart (hypertrophy or dilatation), to effu- 
sion in the pleural cavity on the left side, to pulmonary emphysema 



200 



THE THORAX AND ITS VISCERA 



causing abnormal descent of the lung and diaphragm, and with it 
cardiac hypertrophy. Sometimes tumors in the chest produce a 
similar depression of the apex beat. On the other hand, if the apex 
beat of the heart is felt above the fifth interspace, the heart may 
be raised by pericardial effusions or adhesions following inflam- 
mation, by pleural adhesions or effusions, by abdominal effusion 
(ascites), by tumors, by distention of the colon with gas, and by 
great enlargement of the spleen. Displacement of the apex beat 
to the left is generally associated with downward displacement, 
and is commonly due to hypertrophy of the left ventricle, to pleural 
adhesions, and particularly to pleural effusion on the right side. 
Displacement to the right is due to adhesions and to hypertrophy and 




Fig. 70.— Case of large empyema of left side. The x mark near the right nipple indicates 
the displacement of the apex of the heart to the right. The x mark in tne middle line indicates 
the apex of the heart after the pus had been evacuated. (From a patient in the author's wards.) 

dilatation of the right ventricle, so that the apex beat is felt in the 
epigastrium or against the edge of the sternum. Pleural effusion or 
pneumothorax on the left side may also cause this displacement even 
as far as the right nipple (Fig. 70). (See Plate VIII.) 

The area of the normal apex beat is about one square inch. In 
disease this area often extends over several square inches, generally 
as the result of hypertrophy and dilatation of the ventricles. 

The force of the apex beat in health depends largely upon the 
depth of the chest and the thickness of its wall. It is increased in 
hypertrophy of the hearty when the heart is fully under the influence 
of stimulants, as, for example, digitalis in full doses, in the early 
stages of acute fevers, and in great nervous excitement. If hyper- 



PERCUSSION 207 

trophy is the cause, the apex beat is usually lower, and more to the 
left than normal, and the impulse is more or less diffuse and power- 
fid. r I ne apex beat is decreased in force in cases of dilatation of 
the heart without compensatory hypertrophy, in degeneration of the 
myocardium, in cases of effusion into the pericardium and in the 
presence of pulmonary emphysema, which causes the projection of a 
part of the enlarged lung between the heart and the chest wall. 

Thrills felt in the chest wall over the heart may be due to abnor- 
malities in the blood current when valvular disease or aneurysm is 
present. Thus we find thrills in the precordium, or in the ueigh- 
borhood of the apex, in disease of the mitral valve, both regurgitant 
and obstructive, but they are usually much more marked in stenosis 
than in regurgitation, which latter condition does not cause much 
palpable thrill, as a rule, except in children. A well-marked thrill 
at the apex is usually to be considered a sign of mitral stenosis if 
it is presystolic in time. It is then the so-called "diastolic thrill of 
mitral stenosis." Thrills in the neighborhood of the second right 
costal cartilage indicate an aortic lesion, generally that of aortic- 
stenosis, of aortitis, or of aortic aneurysm. When thrills are felt 
in the tricuspid area, namely, in the midsternal region, or a little to 
the right of it, the lesion is probably tricuspid regurgitation, as 
tricuspid obstruction is very rare. Sometimes a thrill in this area 
is due to aneurysm of the descending part of the aorta. 

Pulsation is felt in the chest wall in some cases of empyema. In 
nearly every instance this pulsation, when it occurs, is found on the 
left side. It is produced by the impulse of the heart against the 
effusion, and occurs in two forms: the internal, in which the effusion 
transmits a heaving impulse to the chest; and the 1 external, in which 
there is a pulsating tumor external in the chest wall. Sometimes 
this is called ''pulsating empyema." 



PERCUSSION. 

Percussion of the chest is commonly performed by placing one 
finger, generally the middle one of the left hand, on the chest wall 
and tapping it on the back with the tip of the bent finger of the 
right hand, the movement of the striking hand being entirely a 
wrist movement. Sometimes percussion is made by directly striking 
the chest with the fingers or palm of the hand (direct percussion). 
Many physicians also employ a percussion hammer with a rubber 
head and a pleximeter, or chest piece, of ivory, celluloid, or glass. 
Glass is by far the best material fdr the chest piece, as it does not 
produce a note of its own when struck by the hammer, as do the 
other materials. The disadvantage of this means of percussion is 



208 



THE THORAX AND ITS VISCERA 



that the physician cannot determine the degree of resistance offered 
by the surface percussed, which is of the greatest service in many 
cases of doubtful character, as, for example, in a case in which 
pneumonia is suspected and the results of the percussion will decide 
the diagnosis. Care should be taken in performing percussion: 
First, that similar points on the chest wall on each side are carefully 
compared; second, that the finger which is applied to the chest is 



Light and heavy percussion pro- 
duce pulmonary resonance 
alone. 



Light percussion develops pul- 
monary resonance. Heavy per- 
cussion reveals dulness due to 
liver under dome of diaphragm. 



Heavy and light percussion gives 
liver flatness. 



Light percussion gives intestinal 
tympany. Heavy percussion re- 
veals liver dulness due to its 
lower edge. 



Light and heavy percussion re- 
veal intestinal tympany. 









k Wk ■ Jr 






11 Mi y ' t 





Fig. 71. — The effects of heavy and light percussion in outlining organs. 

placed in the same relation to the ribs, or interspaces, on each side 
when it is struck; and, finally, in studying the effects of percussion 
the physician should always employ it both during forced inspiration 
and forced expiration, in order to determine the resonance of the 
chest with its full quota of air and when it has only residual air. 

The resonance produced on percussion is due to three things: 
First, to the vibrations of the air in the lungs ; second, to the vibra- 
tions of the chest wall when it is struck; third, to the vibrations in 



PERCUSSION 



209 



the pleximeter placed on the chest. The lasl need be considered 

as a factor only when a piece of celluloid or ivory takes the place 
of the finger, for the finger itself does not vibrate enough to alter 
the note developed. The note produced by vibration of the chesl 
wall can also be excluded as of little importance unless the chesl is 
very pliable and resilient, as in a thin child, and the blow be deliv- 
ered very hard. The most important factor in the production of 
the percussion note is that first named, viz., the vibration of the air 
in the chest caused by the blow delivered on the chest wall. A 
large part of the percussion note depends, therefore, upon the amount 




Fig. 72. — Showing area of partial hepatic dulness (outline) and absolute hepatic dulness 
(solid), merging into cardiac dulness in enlargement of liver. 

of air in the chest, the tension of the chest wall, and the condition 
of the pulmonary tissues. The sound produced when the healthy 
chest is percussed is called the normal pulmonary resonance. 

In percussion, very different results are obtained by the use of 
light and heavy blows, and when percussing the chest it is wise, 
as a rule, to use light percussion, since a heavy blow may produce 
some resonance in a distant healthy part, and so cause the physician 
to overlook a small localized area of consolidation, which light per- 
cussion might discover. Further than this, it is of great importance 
that the sense of resistance offered to the finger placed on the chest 
14 



210 



THE THORAX AXD ITS VISCERA 



in percussion be carefully observed, and many experienced men gain 
more information from this sensation than from the character of the 
note elicited. In consolidation of the lung the elasticity and resili- 
ency of the chest are impaired, and in pleural effusion they are still 
more destroyed. The resiliency and elasticity over cavities are 
marked. The various results produced by heavy and light blows 
are well shown in Fig. 71. 

Percussion of the Respiratory Organs. — On percussing the right 
side of the chest anteriorly in the mammillary line we find in health 
normal pulmonary resonance as low as the fourth interspace or fifth 
rib, at which point the resonance begins to be impaired, so that at 
the sixth interspace or seventh rib we find dulness due to the upper 



Pectoriloquy. 

Consolidated area. 
Fremitus increased. 

Vocal resonance increased. 
Dulness ou percussion. 




Increased vocal resonance 
and fremitus. 

Cavity with cavernous 
breathing and gurgling 
rales. 

Hyper-resonance on per- 
cussion. 

Consolidation — bronchial 
breathing. 

Increased fremitus and 

resonance. 
Dulness on percussion. 

Tubercular infiltration. 

Impaired resonance on 
percussion. 

Congestion— crepitant and 
subcrepitant rales. 



Fig. 73. — Tuberculosis at various stages in one lung, the physical signs depending on the 
stage. The upper part is consolidated, and contains a cavity communicating with a bronchus. 



border of the liver. (See Fig. 71.) The area of partial and absolute 
hepatic dulness is shown in Fig. 72. 

Posteriorly we find on percussion of the right chest that the 
normal pulmonary resonance begins as high as the suprascapular 
area, and ends as low as the tenth or eleventh ribs. It is much less 
resonant as compared with the percussion notes obtained from the 
anterior aspect of the chest, by reason of the thickness of the chest 
wall and the presence of the scapula?. For this reason pulmonary 
resonance is best developed posteriorly at the bases of the lungs 
below the scapulae. Before percussing the back the patient should 
be made to lean forward and fold the arms, in order to stretch the 
tissues and make them tense and as thin as possible. 

We can divide the normal sounds produced by percussion into 



PERCUSSION 



211 



the tympanitic, the dull, and the flat. We can also develop by percus- 
sion of the chest in disease what is known as a "cracked-pot sound." 
A tympanitic sound is best produced in its most typical form by 
percussing the epigastrium when the stomach and colon contain 
some gas. When this sound is produced by percussing the chest it 
is due to one of several causes, such as a large cavity, pneumothorax, 
collapse of the lung, or adhesions of the pleural surfaces. A high- 
pitched note on percussion is also a valuable sign in localizing a 
deep-seated consolidation, for while consolidation produces dulness 
on percussion when it is near the chest wall, it 



s a common thing for 




Fig. 74. — Moderate dulness ou percussion Fig. 75. — Showing high-pitch peruuosion note 

at x over tuberculous infiltration. anteriorly from consolidation posteriorly. The 

shaded area is the consolidated part; z indicates 
the position anteriorly where the percussion 
sound is raised in pitch. 

hyperresonance to be found in the chest over the area which is 
consolidated if healthy lung supervenes. 

If the cavity be in the lung itself, it must be of some size and be 
near the surface to produce a tympanitic note, and, if it communi- 
cates with a bronchus, the character of the note will change when 
the mouth is closed or opened (Fig. 73). If the case be one of 
pneumothorax, with fluid in the chest, changes in the posture of the 
patient will greatly alter the character of the note in a given locality. 

Consolidation of the lung, as in pneumonia and tuberculosis, 
as just stated, generally gives a dull rather than a tympanitic note; 
but if the consolidated area surrounds a very superficially placed 
bronchus, the percussion stroke may produce vibration in the air 
in this tube, and this will cause a note, high pitched in charac- 



212 THE THORAX AND ITS VISCERA 

ter, which varies as the mouth is closed or opened. (See Fig. 75.) 
Collapse of the lung causes a tympanitic or high-pitched note, 
because the comparatively little air in the lung vibrates as a whole, 
its vibrations not being stopped as in health by the tense septa 
and vesicular walls. This note is best elicited in cases of pleural 
effusion over the apex of the chest, into which the collapsed lung 
has been pushed by the effusion. This is sometimes called 
" Skodaic resonance." If the compression is sufficient to consolidate 
the lung, the tympanitic note is lost. This note is not altered by 
opening and closing the mouth. 

The " cracked-pot sound" is produced in an adult by the sudden 
expulsion of the air from a cavity through a small opening by the 




Fjg. 76.— Position of heart partly covered by lungs. (Modified from Aitken.) 

force of the percussion stroke. It occurs on percussing a healthy 
child when its mouth is open, the air being forced by the blow from 
the lung through the glottis. In adults who have a diseased lung 
the cracked-pot sound most commonly results from the presence of 
a cavity, t may also be heard in cases of pneumothorax with a 
fistulous tract opening externally or into a bronchus, in a few cases 
of pleural effusion in thin-chested persons, and, in rare instances, 
before consolidation has occurred in pneumonia. 

In cases of pleural effusion a flat note on percussion is produced 
over the effusion, and it is of very much the same character as the 
sound elicited by percussion of the solid tissues of the thigh. 



PERCUSSION 



213 



Percussion of the Heart and Great Vessels. — On percussing the 
chest anteriorly on the left side at the fourth interspace, it will be 
found that the resonance is decreased by the presence of the heart. 
At the apex of the chest on this side percussion develops normal 
resonance, hut as we descend in the line situated half-way between the 
mammary line and the midsternal line we find an impairment of 
resonance at the third rib which becomes in the next inch of descent 
a very marked dulness, which is produced by the presence of a solid 
organ, the heart. The impairment of resonance is not complete at 
the upper border of the heart, because of the fact that the edge of 
the lung intervenes between the heart and the chest wall, and so the 




Fig. 77. — The cardiac triangles. 



note which results on percussion is neither the normal resonance of 
the lung nor the dulness produced by the presence of the heart 
(Fig. 76). The outlines of the normal cardiac dulness on percus- 
sion are shown by the above diagram, and they form what have 
been called the "cardiac triangles" (Fig. 77). 

The large triangle begins at the level of the second left costal 
cartilage, and extends down the midsternal line to the level of the 
sixth costal cartilage. The base then extends to the apex beat, 
normally situated in the fifth interspace just inside of the clavicular 
line. The hypothenuse of the triangle joins these points. In this 
area we have included the partial and total cardiac Viulness. 



214 



THE THORAX AND ITS VISCERA 



The small cardiac triangle, of absolute cardiac dulness, begins at 
the third costal cartilage and extends to the sixth. The base line 
extends to within one and one-half inches of the nipple, and the 
hvpothenuse joins this point with the third costal cartilage at the 
midsternal line. (See Fig. 77.) The borders of the^ heart really 
extend farther than this, but are not near the chest wall and are 
partly covered by lung tissue as already stated. (See Fig. 76.) 

The greater part of the cardiac dulness on percussion is due in 
health to the presence of the right ventricle, which is nearest the 
chest wall. The right auricle also is well forward, while the left 




Fig. 78. — Position of heart in relation to ribs and sternum, showing the comparatively small 
area of cardiac dulness due to the left ventricle. 

ventricle only fringes the edge of dulness to the left. This is well 
shown in the accompanying diagram (Fig. 78). 

When hypertrophy or dilatation of the heart occurs, it may be 
found that the area of cardiac dulness extends to the right of the 
sternal line and to the left of the long side of the triangle, and the 
apex beat is apt to be displaced downward and to the left. On the 
other hand inability of the physician to discover any such increase 
in the area of cardiac dulness to the left by no means proves that it 
does not exist for the enlarged left ventricle often seems to bury itself 
in the left lung even when this organ is normal in size. If the lung 



PERCUSSION 



21. 



be emphysematous the difficulty of finding the true left outline is 
greatly increased, and in emphysema of the lungs the cardiac 
triangles may be obliterated by the extension of the lung between 
the chest wall and heart. They may also he distorted by reason of 
pleural effusions pressing the heart upward and to the right, or in 
the ease of right-sided pleural effusion the heart may he pushed 
unduly to the left. Pneumothorax may cause similar results, or, 
again, old pleural adhesions and conditions may so displace the 
lungs or heart that the triangles cannot be found. (See Plate \ III.) 




Fie. 79. — Areas of cardiac and hepatic dulness. 



Great distortion of the triangles occurs as the result of pericardial 
effusion (see Fig. SO), but in this case the heart sounds will be distant 
on auscultation and the apex beat very feeble or lost, whereas in 
hypertrophy they are exaggerated and the apex beat forcible. The 
diagnosis of pericarditis, after the stage of dryness and friction sound 
has passed by, is by no means as easily made as some of the text- 
books would make it appear. One of the most reliable signs of 
pericardial effusion is that of Rotch, namely, that any considerable 
dulness in the fifth right intercostal space near the sternum means 
pericardial effusion, provided pulmonary consolidation and pleural 
effusions or adhesions are excluded. The writer has, however, often 



216 



THE THORAX AND ITS VISCERA 



seen this sign present in marked cardiac dilatation; but if, as Ewart 
has pointed out, there is obliteration of the normal acute angle 
between the right border of the cardiac dulness and the line of liver 
dulness, this sign is of value. (See Fig. 79".) In dilatation of the heart 
the area of the apex beat is usually diffuse, and the heart sounds, 
while feeble, are clearly heard. 

In this connection the following summary, prepared by Sansom, 
of the differential diagnosis between dulness due to pericarditis and 
that due to dilatation of the heart, is of interest: 



Outline of dulness 



Rate of development 
of dulness .... 



Impulse and apex- 
beat 



Pericarditis with Effusion. 
Dulness pear-shaped, and en- 
largement chiefly upward. 

Often rapid, and then charac- 
teristic. 

The impulse when present is 
in the third or fourth inter- 
space ; apex-beat tilted up- 
ward and outward, or effaced. 



Dilatation of the Heart. 

Dulness not pear-shaped, and en. 

largement chiefly downward. 

Usually very slow, though a rapid 
dilatation of the heart sometimes 
occurs. 

Impulse can usually be felt to the 
left of the lower end of the ster- 
num or in the epigastrium. 



Usually absent. 



Relation of dulness f Dulness may extend to the left 'i Dulness does not extend to the left 

to left apex-beat . <- of the apex-beat. ) of the left apex-beat. 

Pain over prsecordia 
and tenderness in Y Often present. 
the epigastrium . . J 

Pulsation in the veins f May be present if endocarditis ) Often present when - right heart 

of the neck. 1 complicates. / dilated. 

Usually acute, in course of] Usually chronic ; often associated 

rheumatism, cirrhotic Y with chronic valvular lesions, 

disease, etc. J fatty and fibroid degeneration. 

f Absent unless from some compli- 

t cation. 



Etiology 



• • • -j acute rheu 
[ Bright's di 

Fever { Often present 



The same author also tabulates the facts in the differential diag- 
nosis between increased dulness due to pericarditis and hypertrophy 
of the heart as follows: 



Rate of development 



Impulse, apex-beat 



Pericarditis with Effusion. 
Usually rapid. 

Impulse, when present, is in 
the third or fourth left inter- | 
space, and is feeble ; apex . 
tilted upward and outward, 
or beat effaced. 



Pulse . . . 



Weak and quick 
regular. 



may be ir- 



Hypertrophy. 
Usually slow. 

f Impulse powerful ; if left ventricle 
! hypertrophied, apex displaced 
downward and outward ; if right 
ventricle hypertrophied, apex 
displaced downward and inward 
beat may be in the epigastrium. 

Character of the pulse depends on 
the side of the heart which is 
hypertrophied and the cause of 
the hypertrophy. When left 
ventricle hypertrophied and no 
aortic obstruction or mitral re- 
gurgitation, the pulse is large 
and powerful. 



PERCUSSION 



217 




FiG. SO. — Outline of percussion dulness in extensive pericardial effusion. The light 
shading is the liver dulness. 




Fig. 81. — Diagram of the area of the heart in aortic obstruction and regurgitation. The 
dotted lines show enlargement of the left cavities, especially the ventricle, while the solid 
lines show the normal area. 



218 



THE THORAX AND ITS VISCERA 



The various valvular and other lesions of the heart result in 
alterations in the size of the various cavities without the entire 
viscus being equally affected. Thus aortic regurgitation causes 
enormous enlargement of the left ventricle (dilatation and hyper- 
trophy), and aortic stenosis also causes the same enlargement, as a 
rule, in less degree. Mitral regurgitation causes hypertrophy and 
dilatation of the left ventricle and some enlargement of the left 




Fig. 82. — Area of the heart in mitral stenosis. The dotted lines indicate the enlargement 
of the left auricle and enlarged liver. The solid line shows enlargement of the right cavities. 

auricle, and the left auricle is also enlarged in mitral stenosis. 
Tricuspid regurgitation causes hypertrophy and dilatation of the 
right auricle and hypertrophy of the right ventricle, and mitral 
stenosis often has a similar influence over the right side of the heart 
by damming back the blood into the lungs and right side of the heart. 
The following diagrams illustrate the deformity of the area of cardiac 
dulness under these various conditions (Figs. 81 and 82). 



AUSCULTATION 219 



AUSCULTATION. 

Auscultation of the normal chest reveals in health two sets of 
sounds: the respiratory and the cardiac. 

Auscultation of the Respiratory Apparatus. — The respiratory sounds 
occur in two varieties, namely, vesicular breathing and bronchial 

breathing. The vesicular sound is heard in its most typical form 
over the apices of the lungs anteriorly, the latter at the inferior angles 
of the scapulae posteriorly. We may listen to these sounds by placing 
the ear directly against the chest, or by the use of a single or a 
binaural stethoscope, but neither of these instruments is satisfactory 
for this purpose. The patient must he in an unconstrained position, 
as should be that of the physician, and if the ear is placed against 
the chest, or a single stethoscope is used, the face of the physician 
should always be turned away from that of the patient because the 
breath of a sick person is often very disagreeable and the breath of 
the doctor may be equally annoying to the patient. Care should 
be taken in the use of the stethoscope to see that the edge of the 
bell in its entire circumference is in close contact with the chest wall. 

The respiratory sounds consist, as already stated, in the vesicular 
murmur and the bronchial or blowing sounds, which are sometimes 
designated by the term tubular breathing. In the vesicles the air is 
subdivided into many minute parts, whereas in the bronchial tubes 
it moves along in a column. Whatever may be the actual cause of 
the production of normal "vesicular breathing" we know that when it 
is present it signifies a healthy pulmonary parenchyma, and when 
absent one more or less diseased. 

Bronchial breathing, normal in the bronchial tubes, becomes an 
abnormal sign when it is heard in an area in which vesicular breath- 
ing should be present, as will be shown shortly. 

After determining the fact that the sounds of normal vesicular 
breathing are present in the anterior parts of the chest, or that 
those of bronchial breathing can be heard between the shoulders, 
we next take note as to the relative duration of the inspiratory and 
expiratory sounds. Normally in the perfectly healthy chest the 
ratio of the expiratory sound to the inspiratory sound is as 1 to 3, 
although if the volume of air itself be measured the duration 
of expiration is 6" to 5. In other words, so far as auscultation of 
the vesicular portion of the lung is concerned, inspiration is far 
longer than expiration. Just at this point we learn one of the most 
important points in the physical examination of the chest, namely, 
that while the expiratory sound may be entirely absent in health, 
any marked increase in its length and loudness, so that it equals or 
exceeds the inspiratory sound, is a sign indicative of some diseased 



220 THE THORAX AND ITS VISCERA 

state which impairs the elasticity of the lung, such as early tuber- 
culosis, pneumonia, and emphysema. 

The other variations in the vesicular respiratory sounds differing 
from those of health are harsh, or, as it is sometimes called, puerile 
breathing, and irregular breathing. In children, as the term 
"puerile breathing" indicates, the normal vesicular breathing is 
loud, clear, and harsh, because of the great elasticity of the lung 
and the thinness of the chest wall. If it is exaggerated in a child 
or present in the area of normal vesicular breathing in adults, it 
usually indicates some irritation of the bronchial mucous mem- 
brane. If it is found in the apices of the lungs in a marked degree, 
and expiration is prolonged, it is an important and fairly sure sign 
of early pulmonary tuberculosis, or in acute cases of catarrhal 
pneumonia or influenzal congestion. 

Sometimes physicians speak of " bronchovesicular breathing," 
meaning a breath sound consisting of both bronchial and vesicular 
sounds. It is sometimes heard in a healthy person when he breathes 
superficially, and in disease usually indicates the early stages of 
pneumonia or early tuberculosis of the lungs. It is of value as a 
diagnostic sign only when localized in one part of the lung. This 
harsh breathing of exudation and thickening differs from normal 
puerile breathing in this important particular, namely, that in the 
latter expiration holds its normal ratio to inspiration, whereas in 
disease it is greatly prolonged. 

Irregular, " cog-wheel" breathing occurs in the chest of a healthy, 
sobbing child and in that of an hysterical woman, but it possesses 
pathological significance if it occurs when a full breath is taken, and 
it is often present as an early sign of incipient pulmonary phthisis. 

Bronchial breathing in health is best heard in the posterior part 
of the chest, as already stated, between the scapulae and the seventh 
cervical to the fourth dorsal vertebra. When this bronchial or 
tubular breathing is heard in other parts of the chest it is a sign of 
disease, for while the bronchial tubes are distributed to all parts of 
the lung, the breath sound which is in them is masked by the sounds 
of vesicular breathing and muffled by the lung tissue surrounding 
them. If this vesicular tissue becomes consolidated by disease, the 
vesicular murmur is lost and the solid lung transmits the bronchial 
sounds directly to the ear of the examiner. Bronchial or tubular 
breathing, or, as it is sometimes called, "blowing breathing," heard 
in the part of the lung in which vesicular breathing is normally 
heard, is, therefore, a sign of tuberculous or pneumonic consoli- 
dation (Fig. 83), or of compression or collapse of the lung above a 
pleural effusion. Bronchial breathing is also heard in that area of 
the chest in which vesicular sounds normally predominate, in cases 
of cavity of the lung, because in such a lung the bronchial sound 



MSCULTATIOX 



221 



is transmitted directly to the cavity, and thence to the ear without 
being impaired by the intervention of healthy lung tissue. In 
other words, consolidated tissue and cavities transmit sound better 
than the normal vesicular portion of the lung, which is a combina- 
tion of air and vesicular wall. If the cavity be large, we have a 
loud sound developed by the transmission of the bronchial sound 
into its open space and by the passage of air through it. This is 
called "cavernous breathing." If the cavity is not very large, or is 
peculiarly situated in relation to the supplying bronchus, we have 
what is called "amphoric breathing"— thai is, a sound like that 
produced by blowing over the mouth of an empty bottle. This 



Increased vocal resonance and 
fremitus on auscultation and 
palpation. Dulness on percus- 
sion . . , 




Bronchial breathing. 



Fig. 83. — Pneumonia of the lower lobe with the physical signs of consolidation. 

sound is also rarely heard in cases of pneumothorax in which the 
bronchial tubes, running near to the pleural cavity, transmit their 
sound to the air in the pleural space. 

It is never to be forgotten that in auscultating the chest the two 
sides must be compared, since the well side often gives a standard 
for that affected by disease, and in doing so it must be remembered 
that disease not only modifies the signs in the lung in which the 
morbid process is situated, but also changes the normal signs. Thus 
pneumonia or pleurisy or pleural effusion causes a louder vesicular 
and bronchial breathing on the healthy side than is normal, because 
this lung has to take in more air to make up for the loss of activity 
on the diseased side. Great care should, therefore, be exercised that 
the loud, harsh breathing of the healthy part in such a condition is 
not mistaken for the harsh breathing of disease. 

There are a number of other sounds heard in the chest in cases of 
disease of the air passages. These consist in rales of various kinds, 



222 THE THORAX AND ITS VISCERA 

voice sounds (vocal resonance), friction sounds, and succussion 
notes or sounds. 

Rales are divided into two chief classes, moist and dry. The 
moist are subdivided into the crepitant, or crackling, the fine bub- 
bling, and the coarse bubbling. The dry are called sonorous, or 
sibilant and hissing. Sometimes the sonorous rales are called rhon- 
chi. The fine crepitant rale is best imitated by moistening the thumb 
and finger tip, pressing them tightly together and then separating 
them while they are held near the ear. Another method of imitating 
the fine crepitant rale is to roll the hair where it grows above the ear 
between the thumb and fingers; and still another imitation is the 
crackling of salt when thrown on a fire. This rale is due to the sepa- 
ration of the vesicular walls, which have become adherent because of 
exudate. It occurs, of course, during the latter part of inspiration, 
and is an important sign of croupous pneumonia in its early stages 
before consolidation has occurred. It also is heard in cases of pul- 
monary collapse and edema, but not always in any of these diseased 
conditions. Care should be taken that the fine rales sometimes 
heard in the chest at the bases, posteriorly, in a person who has been 
long in one position in bed, are not thought to be indicative of 
pneumonia, as they are due only to congestion or accumulation 
of secretion due to the dorsal decubitus. 

Fine bubbling rales occur chiefly in the smaller bronchioles and 
the coarse bubbling rales in the larger bronchioles, and they are 
caused by the passage of air through liquid or mucus. These are 
commonly heard in bronchitis and in pulmonary edema in the lower 
parts of the chest, chiefly posteriorly. If such rales are heard ante- 
riorly or in the area for vesicular breathing, they indicate the stage 
of resolution of a pneumonia, or if this disease has not been present, 
or is long gone by, they possess the serious import of breaking down 
of tissue from tuberculosis in the lung. Sometimes these rales are 
limited to inspiration or expiration. In convalescence from an 
attack of asthma they occur with a to-and-fro character, and are 
often musical or tinkling. 

There is another condition in which metallic tinkling is heard 
very clearly, and that is hydropneumothorax. In this condition 
there is a continual dropping of liquid from the apex of the chest, 
or, more correctly, from the compressed lung in the apex of the 
chest, and as the drops fall through the air in the chest they strike 
the surface of the watery effusion with a tinkling sound (Fig. 85). 

Rales are often removed or altered in character, if not crepitant, 
by coughing. 

It has already been pointed out that dry rales may be divided 
into the coarse and sonorous and the small or fine sibilant rales. 
They are produced by the passage of the air, in the large or smaller 



AUSCULTATIOX 



223 



bronchial tubes, through partly inspissated and sticky mucus. If 
they arc sonorous, the larger tubes arc the part involved; if sibilant, 
the small bronchioles are affected. 

If a cavity has formed and liquid is in it, we may hear in the 
chest a peculiar hollow tinkling, called by Laennec "metallic tink- 
ling." These sounds are sometimes heard over the stomach when 
this viscus is in motion and contains a little liquid and air. 

It should not be forgotten that harsh breath sounds made in the 
mouth or in the nose may cause the transmission of rough sounds 
or rales into the lungs, which will mislead the physician in his 
diagnosis if he thinks they arise in the pulmonary tissue-. 




Fig. 84.— Area in which a pleural friction sound is usually heard clearly. 



Friction sounds in the chest depend upon disease of the pleura or 
of the pericardium, generally the former. Normally the visceral 
and parietal layers of the serous membranes glide over one another 
noiselessly, but when they become roughened by disease a sound 
of friction is developed. The friction sound is sometimes so slight 
as to be almost inaudible, and again so harsh as to sound like a 
loud creaking, which not only can be heard, but will convey a sen- 
sation to the hand when it is placed on the chest. As a rule, friction 
sounds due to pleuritis are best heard toward the close of inspiration, 
and occur only in the early stages of the disease, ceasing with the 
development of the effusion and perhaps reappearing as the effusion 



224 THE THORAX AND ITS VISCERA 

is absorbed. The place where the sound is usually most audible 
is near the axilla. (See Fig. 84.) An indistinct pleural friction sound 
may be emphasized, as pointed out by Abrams, if the patient lies 
on the affected side a few minutes, and then quickly sits up and stops 
breathing. The physician places his ear to the chest wall, and directs 
the patient to take a long breath, when the sound is developed. 

If a friction sound is heard at the apex of the chest, tuberculosis 
will often be the cause of its existence. 

Care should be taken that fine rales are not mistaken for friction 
sounds. They can be separated one from the other by the recollection 
of the facts that rales are modified by coughing, are not affected by 
deep pressure on the chest wall, and are usually well diffused, while 
the friction sound is not modified by coughing, is intensified by 
pressure on the chest wall, and is usually limited to a narrow area. 

An excellent imitation of a friction sound is produced by laying 
one hand over the ear, and then firmly stroking the back of this hand 
by the fingers of the other hand. 

Vocal resonance is closely allied to the sensation called vocal frem- 
itus which is felt on palpation, as already described in this chapter. 
It is due to the transmission of the voice sounds down the trachea 
into the bronchial tubes and bronchioles, and thence through the 
various portions of the lungs. If a stethoscope is placed in the epi- 
sternal notch while the patient speaks, and the ear of the examiner 
which is not closed by the instrument is closed by the pressure of 
his finger, the voice of the patient will be very clearly heard. If the 
stethoscope be placed between the vertebral column and the scapula 
posteriorly — in other words, over the bronchial tubes — the voice 
also will be clearly heard, but not as clearly as over the trachea, for 
two reasons: first, because the sound has already been divided into 
the different bronchial tubes, and, second, because the thickness of 
the chest wall muffles it. If the stethoscope be placed over the 
anterior part of the chest toward the sides in the area of typical vesic- 
ular breathing, the sound of the voice will be still more modified, 
because the sound, like the air that conveys it, is now minutely 
subdivided, and the vibrations are decreased by the multitude of 
vesicular walls. Of course, the degree of transmission of vocal 
resonance is governed largely by the character of the voice, and 
for this reason it is more distinct in men than in women. 

If the patient being examined is a man and has a well-developed 
voice, it is usually best to have him speak in a whisper, because the 
full volume of his voice is so great that it will be heard all over the 
chest, and the nice differences between the transmission of the sound 
in the healthy lung and in the diseased area cannot be distinguished. 
Usually we get the patient to speak by asking him to repeat his 
name or count "one, two, three." The unemployed ear of the 



AUSCULTATIOX 



225 



physician should always be closed by the tip of the finger, and the 
counting or speaking should be continued only when the physician 
is actually listening to the chest. 

In diseased states of the lung we find the resonance is increased 
by those changes which aid in the transmission of the sound and 
decreased by those changes which obstruct its transmission. As 
pointed out when speaking of vocal fremitus, a solidified lung and 
the opposite state — namely, a cavity — transmit sound better than 
healthy tissue, which is partly air and partly lung tissue. We find, 
therefore, that the vocal resonance, or the sound of the voice of the 



Heart displaced 
Ai».r brat to the 
righto/ sternum, 



Comjirfssed 
lung 




Tympany 



Succussi" 



on shaking^ 

Flat on i»rcussion with 
loss of vocal resonance and 
\ loss of vocal fremitus. 



Fig. 85, 



Left pyothorax. Metallic tinkling may be produced by the fluid dropping from the 
apex of the chest into fluid below, t, After Maydl.) 



patient when he speaks, is increased in pneumonia, in tuberculous 
consolidation, and in cavity; and is decreased in cases of emphysema, 
or in cases in which a pleural effusion separates the lung from the 
chest and deadens sound. Vocal resonance, however, may be in- 
creased over pleural effusions, particularly the resonance of the 
whispered voice. This is called "Baccelli's sign," and Baccelli 
claims that it serves to separate serous effusions from purulent 
effusions, because in his experience it is absent in the latter class 
of cases and present in the former. 1 

When a cavity is situated near the surface of the lung so that the 
sound of the voice is transmitted to it and from it through the chest 



i This sign is mentioned here for what it is worth. The writer has never been able to use it 
with success. 
15 



226 THE THORAX AND ITS VISCERA 

wall with unusual clearness, the sound so clearly heard is called 
"pectoriloquy." It is usually very marked over a cavity connected 
with a bronchial tube. 

Sometimes when the voice sounds through the chest wall as if it 
were of a bleating character it is called " egophony." Egophony is 
usually heard at the angle of the scapula, near the margin of a pleural 
effusion, and is supposed to be caused by compression and partial 
occlusion of a bronchus. 

Finally, in pyo- or hydropneumothorax, if the ear be placed 
against the chest and the patient is shaken, we have developed a 
splashing or slopping sound, called " Hippocratic succussion." (See 
Fig. 85.) It is not always heard in these cases, and may be devel- 
oped when a large cavity in the lung is partly filled with liquid. 



THE DIAGNOSIS OF RESPIRATORY AFFECTIONS. 

The healthy physical signs, and the variations from the normal 
signs met with in diseased conditions of the lungs, have now been 
discussed. The next step is to group these various signs with other 
characteristic symptoms in order that we may obtain a complete 
picture in the diagnosis of a given disease. 

Croupous Pneumonia. — Let us suppose that a patient, previously 
in health or without any serious pulmonary complaint, is found, 
after a physical examination of his chest, to have rapid breathing, a 
somewhat anxious expression, a bright eye, and a dusky flush on one 
or both cheeks. Palpation discovers a hot, fevered skin, which is 
dry or more rarely moist, and increased vocal fremitus over both 
sides of the chest, more marked on one side than the other. Per- 
cussion reveals impairment of resonance over the area where frem- 
itus was found most increased, and auscultation in this area shows 
bronchial breathing, fine crepitant rales, and increased vocal reso- 
nance. Under these circumstances we have before us the physical 
signs of acute croupous pneumonia. The pulse is apt to be rapid, but 
not so fast as the respiration would lead us to suspect, for it is a 
characteristic of this disease that the respirations are out of propor- 
tion to the pulse. The diagnosis is confirmed by the presence of 
pain in the side affected, by the cough, the rusty, sticky sputum, and 
the history that the illness was sudden in onset and was initiated by 
a chill which may or may not have followed exposure. After a few 
days the rales disappear as consolidation becomes complete in the 
affected part, and the area which gave impaired resonance on percus- 
sion now gives a dull note, while the bronchial breathing in the affected 
part becomes more marked. The lips are apt to be attacked by her- 
pes. With the fall of temperature, or crisis, which may be reached 



THE DIAGNOSIS OF RESPIRATORY AFFECTIONS 227 

by the third to the ninth day, the rales return {rales redux) and 
become more and more loose, coarse, and moist as resolution pro- 
gresses, until the lung becomes entirely clear, and only a slight rough- 
ening of the breath sounds is to be heard. Bad symptoms in such a 
case are delirium, a feeble pulse, a feeble heart with distant heart 
sounds, or one in which the action is labored and irregular. Prune 
juice sputa, or, as the disease progresses, purulent sputa, are bad 
signs also. If the temperature falls to normal about the fifth clay 
and then rises again, forming a pseudocrisis, the attack will probably 
be prolonged. When a child is affected by croupous pneumonia 
it is very common for us to find all the ordinary objective symptom^ 
without any of the physical signs just named. The dulness on 
percussion is difficult of development, because the chest is so resil- 
ient that the percussion blow makes the whole chest resound, and 
it is noteworthy that percussion of the chest on the diseased side 
quite commonly develops a high-pitched tympanitic note such as 
we often find above a pleural effusion. 

Care should be taken in all suspected cases of croupous pneumonia 
that another common cause of the same symptoms does not mislead 
the physician. This cause or condition is acute pneumonic phthisis. 
In many cases only the finding of tubercle bacilli in the suptum, and 
the fact that resolution is delayed, and that finally. the lung breaks 
down and cavities are formed, will permit a diagnosis of acute 
tuberculosis to be made, although the profuse sweats and rapid 
loss of weight may before this occurs reveal the true state. 

There are two areas in the lung often affected very early in 
pneumonia, particularly of the croupous type, and in pulmonary 
tuberculosis, which are apt to be overlooked, namely, the axillae 
and the septum between the upper and middle lobe on the right side, 
an area exposed to percussion and auscultation only when the right 
hand of the patient is placed on top of his head in such a way that 
the angle of the scapula is drawn away from the vertebral line (Fig. 
86). If this is done, the inner border of the scapula will approxi- 
mate the line of the septum, and along this line there will often be 
found in tuberculosis of this portion of the lung marked dulness 
on percussion or, on auscultation, rales, and the other physical signs 
of consolidation, even though the physician is unable to find else- 
where any evidence of local disease to account for the general 
systemic symptoms. Very often careful auscultation of the axillary 
area will also reveal signs not to be found elsewhere, which account 
for the illness, such as those of pneumonia or pleurisy, for here, as 
a rule, the friction sounds of the latter affection are best heard. 

There is another state that gives dulness on percussion, crepitant 
rales, and the other physical signs of pneumonia, namely, pulmonary 
congestion, dependent upon the action of a feeble heart in the course 



228 THE THORAX AND ITS VISCERA 

of prolonged exhausting fevers or mitral disease; but the history of 
the illness, the feeble heart, and the* development of these signs in 
the dependent parts of the chest effectually preclude the idea of any 
acute inflammatory process in the lung. 

Finally, we frequently have after a pulmonary infarction an area 
of consolidation in the lung; but if this be the case, we also have, 




I 



"*«^|pP'. 



Fig. 86. — Area of dulness found in many cases of obscure pulmonary tuberculosis, when 
the arm is raised so that the scapula no longer covers the septum. 

as a rule, a history of recent hemoptysis. This condition is, however, 
comparatively rare. 

The condition of croupous pneumonia cannot readily be confused 
with any other disease except acute pneumonic phthisis, because of 
its characteristic symptoms, but catarrhal pneumonia and tubercu- 
losis of the lung often are confused. 

Catarrhal Pneumonia. — In catarrhal pneumonia the patient usually 
presents a history of recent illness of which the pulmonary state is a 
sequence. The disease rarely begins with the marked and startling 
symptoms of the croupous form, but is insidious and accom- 



THE DIAGXOSIS OF RESPIRATORY AFFECTIONS 220 

panied by a milder but more prolonged fever. Pereussion often will 
not give the positively dull note which can be elicited in croupous 
pneumonia, and only impairment of resonance may be developed. 
There are increased vocal fremitus on palpation and increased vocal 
resonance on auscultation; there are also increased bronchial breath- 
ing and more bronchial rales than in the croupous form, for the 
disease is a bronchopneumonia involving the bronchial tubes and 
adjacent tissues. The signs are generally diffuse, very often heard 
best at the bases posteriorly, and clear tubular breathing, such a> is 
heard in the croupous form, is rarely to be found. The sputum is 
not sticky or rusty; the fever does not end by crisis, but rather by 
lysis; and the lung returns to its normal state very slowly, its con- 
dition often remaining almost stationary for weeks at a time. 

The separation of these symptoms of catarrhal pneumonia from 
those of early pulmonary tuberculosis is practically impossible by 
the physical signs until the case has progressed to a well-advanced 
stage, and the sputum should be well watched for tubercle bacilli. 

Pulmonary Tuberculosis. — Often catarrhal pneumonia merges into 
tuberculosis, and very often the diagnosis of catarrhal pneumonia 
proves to have been made in a case in which the disease is really 
primarily tuberculosis. 

We have to rest the diagnosis of tuberculosis chiefly on the family 
history, the personal history, the fact that recovery does not speedily 
take place, and that the patient loses weight more or less rapidly, and, 
more important than all, the presence as the case becomes well 
advanced of tubercle bacilli in the sputum, and later on yellow elastic 
fibers which indicate a breaking down of the lung tissues. 

In other instances a patient after Complaining of a persistent 
"cold" with more or less cough fails to get better, and suffers from 
loss of appetite, loss of weight, and develops chills and fever, also 
becoming more or less anemic. In such cases it is particularly 
necessary that the physician be on the qui vive for the physical 
signs of pulmonary tuberculosis , as this is the stage in which the 
disease is still curable in most instances. In such patients a slight 
prolongation of expiration, with harsh inspiration, and impairment 
of resonance on percussion, may be the only, yet very important, 
physical signs. 

If the malady be tuberculosis and progressive, we soon find in the 
chest and sputum signs which make the diagnosis clear. On 
inspection the costal breathing is less than normal; the hand placed 
upon it feels, when the patient speaks, that there is not only in- 
creased fremitus, but a bubbling feeling from coarse rales, and 
auscultation also reveals loose rales, the signs of the breaking down 
of lung tissue. Finally, when a cavity is developed the percussion 
sound over it becomes high-pitched, and, if the cavity be large, 



230 



THE THORAX AND ITS VISCERA 



almost tympanitic, although all around it dulness may be present. 
If the cavity is large, it will often be found that it is possible to 
develop a still more tympanitic percussion note if at the same 
time that the chest is percussed the patient holds his mouth open. 
This is called "Wintrich's change of note." The breath sounds 
now become more tubular or amphoric, and vocal resonance may 
be increased to such an extent that bronchophony or pectoriloquy 
becomes marked even in that part of the lung in which in health 
the vesicular sounds are heard most typically (Fig. 88). Prolonga- 
tion of expiration is also present, and sweats, irregular hectic fever, 
and great loss of flesh ensue. 







Fig. 87. 



Areas of fine moist rales in early stages of tuberculosis of apices of lungs with 
impaired resonance on percussion and prolonged harsh expiration. 



When there is fibroid phthisis of the lungs, inspection of the thorax 
often shows marked retraction of one side of the chest, more often 
the left side in front near the apex. The supraclavicular fossa and 
the costal interspaces are apt to be retracted, the scapula drawn 
nearer the spine, and that side of the thorax is poorly expanded on 
inspiration. The respiratory murmur is feeble and distant, and 
resonance on percussion is below normal. If secondary pleural con- 
tractions occur, the heart may be drawn from its normal position 
and the other lung is apt to be emphysematous. This form of pul- 
monary tuberculosis is usually very slow and lasts for years. 

In striking contrast to the form just described is acute pneumonic 
phthisis, which often begins with the suddenness of an acute croupous 



THE DIAGNOSIS OF RESPIRATORY AFFECTIONS 231 

pneumonia, with a chill, blood-tinged sputum, and pain in the chest. 
When the consolidated lung fails to undergo resolution the sputum 
is examined and tubercle bacilli reveal its true nature. In other 
cases an attack of true croupous pneumonia sets free tubercle bacilli 
which have been walled oft' from the rest of the lung, and so pre- 
cipitates acute pulmonary tuberculosis. 

In some cases of suspected pulmonary tuberculosis the Rontgen 
rays can be used with great success in aiding difficult diagnosis. It is 
best to employ the fluoroscope rather than the radiograph, since 
with the former different parts of the chest can be rapidly compared, 
and the focus readily changed for deep and superficial tissues. ( !on- 
solidated areas are dark and shadowy; cavities are light surrounded 




Pig. 88. — Case of pulmonary cavity due to tuberculosis. The central ring is the area giving 
the physical signs of cavity, with cavernous breathing and whispering pectoriloquy, and the 
outer ring that of consolidation (dulness), with rapid breaking down of the lung tissue (moist 
rales). 

by shadow. So, too, abscess of the lung produces a distinct shadow 
in many cases. 

Finally, it is to be recalled that mitral stenosis or even regurgi- 
tation, may, by producing engorgement of the lung, produce physical 
signs closely resembling pulmonary tuberculosis, for there are con- 
tinued cough, dyspnea, blood-spitting, and loose rales on ausculta- 
tion. The absence of tubercle bacilli, and the presence of large cells 
filled with brown pigment in the sputum show the cause to be cardiac. 

Pulmonary Abscess. — The history of the case and its symptoms 
are our chief means of separating pulmonary abscess from pulmonary 



232 THE THORAX AND ITS VISCERA 

tuberculosis with the development of cavity, for the physical signs 
are about the same. In cases of abscess we find that the patient has 
suffered from pneumonia or from pyemia with embolic infarction. 
In other cases discharges from the nose and throat entering the 
lungs produce such lesions. The symptoms of abscess, which sepa- 
rate it from cavity due to tuberculosis, are as follows: in abscess 
the lesion exists in the lower lobe, as a rule, while the tuberculous 
cavity is usually found at the apex or in the upper lobe. The consti- 
tutional disturbance in abscess is often very slight, whereas in 
tuberculosis it is usually severe. In abscess the sputum is copious 
and purulent, and often coughed up in gushes, whereas in tubercu- 
losis it is often scanty, and not markedly purulent, as a rule. Again, 
in the last-named disease tubercle bacilli may be found, but they 
are absent in abscess unless tuberculous infection is simultaneously 
present. 

The use of the fluoroscope is of great value in localizing the pus 
in some cases. 

Pulmonary Gangrene. — If the patient has the signs of cavity of the 
lung, and in addition an exceedingly fetid breath, with great wasting, 
the case is one of pulmonary gangrene. Gangrene is usually found 
at the base of one lung, as is abscess. The sputum is usually 
brownish. 

Bronchiectasis with fetid breath is occasionally met with, but the 
fetor after coughing is never so exceedingly offensive as it is in cases 
of gangrene. 

Pulmonary Edema. — The physical signs of pulmonary edema may 
develop suddenly as a result of an injury to the vagus, or in acute 
disease of the kidneys, lungs, or heart. Their onset is insidious, 
but the rapid breathing, the crepitant rales, the limitation of 
these signs chiefly to the lower part of the chest, the bilateral 
character of the signs combined with dulness on percussion, the 
absence of fever, the frothy sputum, and, it may be, the associated 
presence of renal or cardiac disease, all point to the true state of 
affairs. Such a state not rarely develops in the course of pulmonary 
congestion in old persons, particularly if influenza is the cause. 

Pleuritis. — Let us suppose that a healthy man is seized with pain 
in the thorax and a chill followed by fever. An examination of his 
thorax will reveal on inspection deficient breathing on the affected 
side, which is fixed because of pain produced by the inflamed 
pleural surfaces moving over one another on inspiration. Exag- 
gerated breathing will be found on the opposite side to compensate 
for this fixation, and auscultation on the painful side will reveal a 
friction sound, probably best heard in the axilla. (See Fig. 84.) 

Pleural Effusion. — The signs of pleural effusion are impaired 
mobility, or fixation of the affected side and obliteration of the 



THE DIAGNOSIS OF RESPIRATORY AFFECTIONS 



233 



interspaces where the fluid exists. The chest is flat on percussion at 
the most dependent part of the pleural sac, namely, at the base of the 
lung posteriorly. This area of flatness on percussion gradually rises 
higher and higher until the effusion is completed. It extends ante- 
riorly, and may be demonstrated as well here as it can be posteriorly 
and laterally, although, if the patient lies on his back or is partly 
recumbent, the entire anterior surface of the chest may be hyper- 
resonant, owing to the fluid leaving the front of the chest and going 




Fig. 89. — Right-sided pleural effusion. The area of flatness on percussion in the thorax 
merges with that of liver dulness, and the lower border of the liver is below its normal level. 
The apex beat is displaced to the left at x. The circle represents Traube's semilunar space, 
which is obliterated in left-sided effusion, but not in right-sided effusion. 

to the more dependent parts. In other words, in cases of non- 
sacculated serous pleural effusion changes in the position of the 
patient cause alterations in the area of flatness on percussion, unless 
the effusion is large enough to fill the chest entirely, when, of course, 
it is immovable. Inspection will show an increase in the size of 
the chest on the diseased side, with bulging of the intercostal 
spaces. 

A curious yet important point in this connection is the fact that 



234 THE THORAX AND ITS VISCERA 

the line where flatness on percussion ceases at the top of the effusion 
posteriorly is wavy or sigmoid (S-shaped). Above the level of the 
effusion percussion over the compressed lung gives a somewhat 
hollow note or hyper-resonance, called "Skodaic resonance," and the 
sense of resistance to the percussed finger is less at this point than 
over the effusion where the resistance is great. Percussion and 
palpation will reveal the lower margin of the liver depressed if the 
effusion is on the right side. (See Figs. 89 and 90.) Inspection and 
palpation will show the apex beat of the heart displaced to the right 
and downward in cases of effusion into the left pleura, and to the left 
in cases of right-sided effusion. Again, if the effusion be on the left 
side, it will be found on percussing "Traube's semilunar space/' a 
space directly in the mammillary line and a little below the nipple 
that the usual tympanitic resonance normally found in this area is 
extinguished through the downward pressure of the fluid. 

In many cases of pleural effusion careful percussion posteriorly 
at the base of the opposite side of the chest from that of the effu- 
sion close to the spine will reveal marked dulness. This area of 
dulness is triangular in shape with the base of the triangle near the 
diaphragm and its apex several inches up the side of the vertebral 
column. This is called Grocco's sign or the "paravertebral triangle 
of dulness of pleural effusion." 

In auscultating the chest in the area in which flatness has been 
developed by percussion the breath sounds are very indistinct, 
except in the back near the vertebral column, where there may be 
marked blowing breathing. If the patient speaks, there will be 
found loss of vocal resonance and of fremitus over the effusion, but 
along the margin of the spine on the diseased side there may be 
heard in some cases bronchophony, or even the bleating voice sound 
called egophony. 

It is a noteworthy fact, however, that the physical signs on aus- 
cultation vary with the method of examination which is employed, 
for if the stethoscope is used the breath sounds are often inaudible, 
whereas, if the unaided ear is used bronchial breathing may be dis- 
tinctly heard. The presence of bronchial breathing over an area 
supposed to contain fluid does not negative this diagnosis if the 
unaided ear is employed. While it seems paradoxical that sounds 
can be heard with the naked ear which are inaudible with an aided 
ear the paradox is explained by the fact that when the stethoscope is 
used only a very limited portion of the thoracic contents is auscultated. 

If the effusion be accompanied by pneumothorax (see next page), 
we will find three sets of physical signs, namely, those of effusion, 
which will be at the lowest part of the chest, next above this an area 
in which percussion gives a clear tympanitic note due to the air in the 
pleural cavity, and above this the physical signs of the compressed 



77/ A' l)l.\(l\OSIS <)E RESPIRATORY AFFECTIONS 



235 



lung in the apex of the chest cavity. In this condition we may also 
hear succussion or splashing sounds, if the patient is shaken while the 
physician's ear is against the chest wall, and the metallic tinkling, 
or dropping sounds, as the fluid falls from the top of the chest cavity 
into the effusion. (See Fig. 85.) Again, we may use what has been 
called "coin percussion." This consists in having an assistant place 
a large silver coin against the chest wall on the diseased side ante- 
riorly, and then the physician listens at the posterior aspect of the 
chest, his unused ear being closed by his finger. The assistant now 
strikes the silver coin with the ^(\^e of another silver coin. It the 




Fig. 90. — Showing at x mark the so-called area called Traube's semilunar space, where in 
health percussion gives a tympanitic note, which becomes flat in left-sided pleural effusion. 
The solid block represents hepatic and cardiac dulness. 

coins be struck together below the surface of the effusion, very little 
of the metallic sound will be transmitted through the chest. If the 
coins are struck together at the level of the layer of air, the sounds 
come through the chest cavity with startling clearness; but if at the 
level of the lung, they are less clearly heard than at the level of the 
air, but more so than at the level of the effusion. 

The reasons for this are obvious, for the liquid prevents transmis- 
sion of the metallic sounds, as does also to some extent the com- 
pressed lung at the apex of the chest, whereas the space filled with 
air conveys J;he sounds directly to the ear, 



23G THE THORAX AND ITS VISCERA 

Finally, if the effusion is absorbed by unaided nature, the area 
of flatness on percussion becomes less and less from above down- 
ward, the expansion of the chest on inspiration increases, the inter- 
spaces cease to bulge, and the friction sounds may return for a brief 
period. 

Particular attention should be called to the possibility of pleural 
effusions coming on insidiously. There is probably no other massive 
pathological change anywhere in the body so often unsuspected or 
overlooked, and it is noteworthy that, when pleural effusion is insidi- 
ous in its onset and devoid of prodromes, it is often due to an undis- 
covered tuberculosis, whether the exudate be found to be serous or 
purulent. Again, the fact that tubercle bacilli cannot be found in 
the effusion when it is aspirated in no way proves that the effusion 
is not tuberculous in origin, since they are rarely found in the fluid 
even when tuberculous pleurisy is most active. 

Serous pleural effusion, single or double, may occur as part of the 
dropsical condition in renal or cardiac disease, from disease of the 
blood itself, or it may result from thrombosis of the vena azygos. 
The latter cause is particularly apt to come on in patients suffering 
from typhoid fever or other exhausting diseases. A right-sided 
effusion may arise from heart disease which primarily enlarges 
the right side of this \iscus which in turn presses upon the root of 
the right lung and so compresses the vena azygos major. 

Transudations can be separated from the effusions due to inflam- 
mation by the method of Pohl and Rosenbach. This consists in 
withdrawing some of the fluid by an aspirating needle after the 
patient has received doses of iodide of potassium. A few drops of 
fuming nitric acid are added to the fluid, and it is then agitated with 
chloroform, when, if the effusion be a transudation, the iodine will 
be seen of a red color sinking to the bottom of the test tube with the 
chloroform. If it be an inflammatory exudate, the iodine will not 
be passed into the effusion. 

Additional information may be obtained by the following methods, 
none of which, however, are. positive but only indicative in their 
results. The first consists in an estimation of the proportion of leuko- 
cytes contained in the aspirated fluid (cytodiagnosis). It may be 
said that if the fluid contains a relatively large proportion of poly- 
morphonuclear cells (60 to 90 per cent.), its exudation has resulted 
in all probability from infection by the pneumococcus, the strepto- 
coccus or the staphylococcus, and that there has been an acute 
inflammation of the pleura. In such cases small masses of fibrin 
may be found in the fluid. The number of polymorphonuclear cells 
and the quantity of flakes of fibrin are, as a rule, in direct proportion 
to the severity of the inflammation. If the fluid contains a relatively 
large proportion of lymphocytes, it is probably due to tuberculous 



THE DIAGNOSIS OF RESPIRATORY AFFECTIONS 237 

infection. Such findings are only of value as confirming an opinion 
based upon other points in the history of the case, or those which 
may have been discovered by a careful study of the physical signs, 
and they are liable to mislead if too much reliance is placed upon 
them. Thus, in some cases of tuberculous infection a large propor- 
tion of polymorphonuclear cells may be present in the first fort- 
night during which the effusion has taken place, although later they 
diminish as the lymphocytes increase. Again, if the infection by 
the tubercle bacillus is mixed, that i> t<> say if. a- so often happens, 
other microorganisms are active, such a- the pnenmococeus, then the 
presence of these organisms may in a case of tuberculosis cause a 
polymorphonuclear leukocytosis. 

The technique advised for this method of examination i> as 
follows : 

The fluid having been drawn into a sterile vessel several sterile 
glass balls are placed in it and shaken to break up any clot which 
may, by forming, entangle the leukocytes in its meshes. The con- 
tents of the vessel is centrifugalized for five minutes, after which the 
supernatant fluid is entirely decanted, only a few drops remaining 
in the vessel or test tube. From this remaining fluid and sediment 
after they are thoroughly mixed by stirring them with a platinum 
loop, a drop is removed by means of the loop and a smear i> made 
between tw T o cover-glasses as in ordinary blood examinations. After 
the smear is dry the cover-glass is dipped in alcohol to fix the cells, 
which are then stained by immersing the glass for thirty seconds in 
a fluid composed of Wright's blood stain three parts, and pure 
methyl alcohol one part. The stain is then diluted by adding to the 
cover-slip a few drops of water, and is allowed to remain in contact 
for two minutes, when the glass is washed with pure water several 
times. After this, it is dried by waving it over a Bunsen flame, at 
such a distance that the fingers can stand the heat. The cover-glass 
is now mounted in xylol balsam and placed under an oil-immersion 
lens. 

A third method of gaining some idea of the cause of an effusion 
consists in studying its specific gravity. If the effused fluid has a 
specific gravity of from 1.010 to 1.020 it is probably the result of an 
acute infection by the pnenmococeus or the streptococcus or staphylo- 
coccus; whereas if its specific gravity is as low as 1.00S it is probably 
a transudate. 

A fourth method nearly related to that just named is the estimation 
of the albumin content of the fluid. There are several methods by 
which this estimation can be made. Only one of them lends itself 
to employment by the practitioner, namely, that of Brandberg. 
That of Kjeldahl and that of Reuss are too complicated. 

Brandberg's method consists in a determination of the rapidity 



238 THE THORAX AND ITS VISCERA 

with which cloudiness appears at the point of contact of nitric acid 
and the fluid tested as in urinary analysis. When the cloud develops 
in from two and a half to three minutes the fluid contains about 
0.033 per cent, of albumin. If more albumin than this is present the 
cloudiness develops in a shorter time, and if less than this is present 
a longer period of time elapses before the cloud appears. Effusions 
due to inflammatory processes contain 4 per cent, or more of albu- 
min, whereas those due to transudation contain from 1 to 3 per cent. 
A fallacy underlying this method depends upon the fact that an 
inflammatory process may be responsible for a part of the fluid 
when another part is the result of transudation resulting from venous 
stasis produced by pressure arising from the inflammatory process. 
In this manner a low albumin content is developed. 

A fifth method is by determining the freezing point of the fluid. 
This requires so much apparatus and special skill that it is not prac- 
tical for the average physician. This is called "cryoscopy." 

A sixth method is called "inoscopy," or the determination of the 
presence of tubercle bacilli by bacteriological methods that do not 
lend themselves to the hand of the general practitioner since the 
fluid and its contents requires careful treatment before the staining 
for tubercle bacilli is attempted. 

If on aspirating the fluid in the chest it is found to be hemorrhagic 
in character, the cause may be one of the diseases which produce 
marked asthenia, notably carcinoma, nephritis, one of the acute 
infectious diseases in a malignant form, or tuberculosis. The cancer 
may or may not be in the chest. Rarely such an effusion occurs in 
otherwise healthy men without these causes. The possibility of the 
hemorrhagic effusion being due to a leaking aneurysm, or to leakage 
from an ulcerated bloodvessel in tuberculous disease of the lung is 
to be remembered. 

Sometimes interlobar pleurisy develops and effusion of fluid or of 
pus takes place in such a position that it lies between the two lobes 
without escaping into the general pleural cavity. Under these con- 
ditions the symptoms of an ordinary pleuritis may be present, and 
the physical signs will consist of an area of flatness on percussion, 
which is sharply outlined, and is bordered above and below by an area 
of high-pitched resonance on percussion, and tubular breathing due 
to compression of the lung. 

Empyema. — If the effusion is purulent, the patient is apt to lose 
flesh and strength, to have chills, fevers, and sweats, and to present 
all the evidences of an accumulation of pus in some part of the body. 
Particularly is this result apt to follow a pleurisy complicating one 
of the acute infectious diseases, such as scarlet fever, typhoid fever, 
pneumonia, and in many cases in which tuberculosis is responsible 
for the illness. In children empyema is not so serious as it is in adults. 



THE DIAGNOSIS OF KKSI'IRATORY AFFECTIONS 239 

In the former it is usually due to the pneumococcus, in the latter to 
the streptococcus. The following statistics, compiled by Xetter, 
show the frequency with which these organisms produce empyema 

in adults and children: 

Children. Adults. 

Pneumococcus 53.0 17.3 

Pneumococcus and streptococcus . 3.6 2.5 

Saprophytic organisms 10.7 . . 

Staphylococci 1.2 

Tuberculosis 14.3 25.0 

Streptococci 17.7 53.0 

Empyema may also be due to the bacillus typhosus, the colon 

bacillus, the microorganism of influenza, the gonococcus, and actino- 
mycosis. 

Pneumothorax. — The development of sudden dyspnea and thoracic 
pain, with pallor and cyanosis, a subnormal temperature and a 
rapid pulse, during the course of a case of tuberculosis of the lung in 
particular, should lead us to suspect pneumothorax. Inspection 
shows distention of the affected side, bulging of the intercostal spaces. 
and a sensation of distention of the chest to the physician's hand. 
The act of respiration moves the involved side but slightly, while the 
opposite side is moved greatly. The apex of the heart is displaced 
and percussion gives a loud hollow note. Auscultation of the affected 
side reveals absence of breath sounds, and the hyper-resonance on 
percussion with absence of respiratory murmur makes a very pathog- 
nomonic combination of symptoms. [Metallic sounds are often 
elicited in this condition arising from unknown causes. It will be 
found that if the pleximeter is struck with the handle of a percus- 
sion hammer, while the physician auscults the chest elsewhere, a 
clear distinct metallic sound is transmitted to the ear. When a 
pneumothorax communicates freely with a bronchus we often have 
gurgling or bubbling sounds due to bronchial secretion, or if pus is 
in the thorax, we find moist rales in the bronchial tubes and puru- 
lent expectoration. It is remarkable how differently patients suffer 
when affected by pneumothorax. Some are in the most urgent 
dyspnea, but others after a very short time seem to be able to take 
some exercise without grave embarrassment. 

Bronchitis. — If after exposure to cold there is a sense of soreness 
in the chest, with more or less oppression and a hard cough, which 
seems to tear the bronchial tubes, the cough not being associated 
with expectoration, and the febrile movement but moderate, we 
suspect the presence of an acute bronchitis; a diagnosis which will 
be confirmed if we find the following physical signs : 

There is marked roughening of the breath sounds all over the 
chest, particularly over the bronchial tubes at the back, between 



240 THE THORAX AND ITS VISCERA 

the scapulae, without any increase in vocal resonance and fremitus 
or any impairment of resonance on percussion. As the disease 
progresses these sounds of harsh breathing give way to rales, which 
are at first fine and moist, then coarse and sonorous, as the second 
stage, or stage of secretion, develops; and, finally, they decrease 
little by little, as health is approached and the mucus is expelled by 
coughing. Care should always be taken to determine in examining 
a case of suspected bronchitis that the symptoms are not due to a 
bronchopneumonia. 

Should the case become chronic, the sounds of coarse and more 
or less sonorous rales will persist and become constant. Such cases 
usually become worse in winter, and the sputum is sometimes very 
profuse (bronchorrhea). 

The physician should always be careful in these cases to see to 
it that renal disease or a feeble heart is not the cause of the bron- 
chial disorder. The health suffers but little in simple chronic 
bronchitis; but if bronchiectasis develops it may be much impaired. 

Too often the careless diagnosis of chronic bronchitis is made 
when the trouble is due to pulmonary tuberculosis or a feeble heart. 

Under the name "putrid bronchitis" we have a state in which the 
sputum is foul and expelled in a liquid form, in which float little 
yellow plugs (Dittrich's plugs). This condition may end in pul- 
monary gangrene or cause metastatic abscess. 

Emphysema. — The presence of a barrel-shaped chest, with almost 
immovable walls and marked abdominal breathing, points to the 
presence of emphysema of the lungs, and this opinion is confirmed 
if on auscultation of the chest we find marked prolongation of expi- 
ration, diminished vocal resonance and fremitus, and increased reso- 
nance on percussion. The face is often quite cyanotic, the superficial 
veins of the neck turgescent, the abdominal respiratory movements 
abnormally great, and the superficial veins in the epigastrium 
enlarged. If bronchitis or bronchiectasis is associated with the 
emphysema, as is frequently the case, we find more or less marked 
rales all over the chest, particularly posteriorly. Sometimes a systolic 
murmur can be heard over the tricuspid area, due to regurgitation 
on the right side of the heart. Cardiac dulness is generally obliterated 
by the enlarged lung, and the apex beat cannot be felt except in the 
neighborhood of the ensiform cartilage or in the epigastrium. Both 
the hepatic and splenic dulness are found to begin and extend lower 
than normal, owing to the expansion of the lung. We may also find 
accentuation of the second sound in the pulmonary artery. The 
tricuspid regurgitation not rarely develops as a result of a damming 
up of the blood in the right ventricle. 

Asthma. — If it is asthma, there will be labored breathing in which 
all the accessory muscles of respiration in the neck and trunk aid 



THE DIAGNOSIS OF RESPIRATORY AFFECTIONS 241 

the ordinary respiratory muscles. The posture of the patient will 
usually be that of sitting up in bed and somewhat leaning forward. 
The face will be flushed, the vessels of the face and neck turgid, and 
the lips may be cyanotic. Often the patient, while sitting up, sup- 
ports himself by resting on his hands, which are placed at his side 
in order to raise his shoulders and fix the chest walls for contraction 
of the muscles which are endeavoring to drive out the air, for it is 
to be remembered that the respiratory difficulty in asthma depends 
more upon the fact that the patient cannot empty the lungs than upon 
the fact that he cannot fill them. As a matter of fact, they are too 
full of air which has been used. 

Inspection not only shows these signs in asthma, but also reveals, 
in cases in which emphysema has not developed to such an extent 
as to cover the heart with the lung, that the apex beat is diffused 
and the heart laboring. Palpation reveals little except when coarse 
rales are present in large numbers, when some bubbling may be felt. 

Percussion usually gives an increased resonance, because the chest 
is inordinately full of air, and auscultation reveals very loud blow- 
ing breathing, musical notes, or squeaking or creaking noises, both 
on inspiration and expiration. Finally, as secretion begins to be 
established, musical and cooing rales may be heard, in well-marked 
cases, all over the chest before the ear is placed against the patient. 
At first these rales are heard chiefly on expiration, but very shortly 
they occur equally loudly on both inspiration and expiration. 

If on auscultating the chest we find it filled with musical and cooing 
rales heard in every part, although most marked in the bronchial 
tubes, we may be fairly sure that an attack of asthma is about pass- 
ing away; but if, on the other hand, the attack is beginning, the 
manifest difficulty in breathing, the prolonged expiration, with com- 
paratively few rales, the harsh bronchial sounds, and the general 
objective symptoms of the case will explain the cause of the pul- 
monary condition. Toward the end of the attack coughing brings 
up a limited amount of sputum, which contains Curschmann's spirals 
and Charcot-Leyden crystals. (See chapter on Cough and Ex- 
pectoration.) 

As asthma is a symptom, not a disease in itself, the physician 
should always examine the nose, with the object of discovering some 
source of reflex irritation in the nasal mucous membrane, or test the 
urine to discover whether renal disease is present, or the heart to 
determine if a cardiac lesion accounts for the symptoms. Sometimes 
gastric disorder is responsible for the attack. 

Care should be taken that a catarrhal pneumonia developing after 
an attack of asthma is not overlooked until the patient is danger- 
ously ill. 

When a patient is seized with a violent attack of dyspnea its cause 
16 



242 THE THORAX AND ITS VISCERA 

may be asthma, a foreign body in the air passages, or laryngeal 
spasm. 

Foreign Bodies in the Air Passages. — The dyspnea due to a foreign 
body in the air passages, whether it be a piece of meat or a false 
membrane, is quite different from that of true asthma, for in this 
case the difficulty is commonly in the entrance of air. The onset 
of the attack is usually sudden, and inspection will show that on 
inspiration the costal interspaces are greatly drawn in, as is also the 
epigastrium. There will be practically no signs in the chest which 
are not evidently due to the efforts at forced breathing, and a history 
of having had a foreign body in the mouth or of some laryngeal dis- 
ease will usually be obtainable. Obstruction may, however, be pres- 
ent, and the history of a foreign body be absent in cases in which an 
abscess has burst into the air passages from the mediastinum or 
through the posterior pharyngeal wall. In such a case, however, 
there would be, in all probability, purulent expectoration. 

Laryngeal Spasm. — Laryngeal spasm producing difficult breathing 
causes symptoms precisely like those of a foreign body in the larynx, 
except that in spasm the cough is often constant and is very brassy 
or ringing. The patient will show by a gesture with his hand that the 
obstruction is in the larynx, if unable to speak. Such obstruction 
when seen in children is, as a rule, due to spasmodic croup, and, if 
so, probably depends upon one of three causes, namely, laryngeal 
catarrh, rickets, or digestive disturbance. If in an older person, it 
is probably due to aneurysm pressing on the recurrent laryngeal 
nerve, to a laryngeal crisis in locomotor ataxia, or to growths in the 
mediastinum producing pressure on the nerve trunks going to the 
laryngeal muscles. Sometimes great enlargement of the retrobron- 
chial glands will cause reflex laryngeal spasm. 

Tumors of the Chest. — Tumors occur in the chest generally as 
mediastinal growths, and are most commonly sarcomata or lymph- 
adenomata. There will be found, if the growth be large, evidences 
of its pressure upon the chest wall, such as bulging and dulness on 
percussion over the swelling. This level of dulness is unaltered by 
changing the posture, as it may be in pleural effusion. Generally 
there will be evidence of pressure on the bronchial tubes, which 
causes dyspnea, and of pressure on the thoracic vessels, which pro- 
duces signs of impaired circulation as shown by cyanosis, venous 
engorgement, and flushing of the skin of the face and neck. Often 
such growths cause pleural effusions by pressure on the bloodvessels, 
or produce pulmonary consolidation by causing an exudation in 
the lung tissue. 

The diseased conditions from which it is necessary we should 
distinguish mediastinal growths during life are as follows: (1) 
From aneurysm; (2) from abscess; (3) from pleural effusion; (4) 



THE DIAGNOSIS OF RESPIRATORY AFFECTION'S 243 

from chronic pneumonia. There are several subdivisions of these 

diseases that might be made, hut to all intents and purposes these 
are sufficient. Pericarditis may, perhaps, be named as the fifth 
lesion to he thought of. On general principles it may he said that 
primary mediastinal growths are so rare that they can he excluded 
on this ground in many cases. 

Deeply seated aneurysm in the thorax is sometimes extremely 
difficult of absolute diagnosis from tumor that hut few rules can he 
laid down for its differential diagnosis from growths in the medi- 
astinum, for deeply seated aneurysm in this region cannot he said to 
possess any pathognomonic symptoms. The various portions of 
the aorta in which aneurysm occurs make its symptoms different in 
almost every case, and we are forced to rely more upon general con- 
ditions than absolute signs. Thus, if a patient lias no direct symp- 
toms of aneurysm, and none of those conditions present which we 
know predispose to such a lesion, such as atheroma of the blood- 
vessels, or syphilis, or a history of violent exertion or severe toil, we 
may with a certain degree of assurance look farther for symptoms <>f 
mediastinal trouble of another sort than aneurysm. (See Aneurysm, 
in this chapter.) 

Unfortunately, the most common age for aneurysm is much the 
same as that for mediastinal disease, although mediastinal disease 
seems to occur more frequently in youths than does aneurysm, or, 
in other w T ords, is scattered over a wider range of years. The pain 
in some cases of aneurysm is often more violent than that of any 
other thoracic lesion except angina pectoris. If the aneurysmal 
sac be large enough to give a wide area of dulness on percussion, 
there ought to be an expansile movement. Hemoptysis is not in 
any way a differential sign, since in the one case it may he due to 
aneurysmal leakage, and in another to ulceration. of small blood- 
vessels by pressure exercised by a tumor, be it aneurysmal or malig- 
nant, or even benign. Aneurysm is relatively the more frequent 
lesion. (See latter part of this chapter.) 

Mediastinal ahscess is to be separated from mediastinal tumors 
with care. In the first place, in ahscess we generally have a history 
of infection, or, if the case be one of cold ahscess, it is commonly 
associated with a history of struma or spinal disease. If the ahscess 
be acute, there is generally the history of pain, followed by a chill 
more or less severe, and fever; or, if cold, then we frequently have 
irregular febrile movements, with loner-continued anorexia and loss 
of flesh. Cold abscess, too, is generally in the posterior mediastinum, 
while acute abscess generally occurs in the anterior space. 

Pulsation may frequently occur, owing to the transmission of the 
aortic or cardiac impulses, and affords no better diagnostic point 
here than elsewhere. In some cases where the presence of aneurysm 



244 



THE THORAX AND ITS VISCERA 



is extremely doubtful and the likelihood of abscess extremely prob- 
able, an exploratory needle may be used, either through a hole drilled 
in the sternum or passed between the ribs; but a careful review of 
the history of the case should certainly always be made and used as 
a basis from which to draw conclusions. 



AUSCULTATION OF THE HEART AND VESSELS.. 

On attempting to study the heart sounds, we usually auscult the 
neighborhood of the apex beat and find, if the heart be healthy, two 





® <E> 

<8> 



Fig. 91. — Showing the areas in which the various heart sounds are best heard in health. 
A is the area for the aortic valve ; P, that for the pulmonary valve; T, for the tricuspid valve; 
and M, for the mitral valve. The pulmonary circle is a little high. 

sounds, occurring one immediately after the other, which resemble 
"lub dup," the "lub" being the so-called first sound of the heart, 
produced by the contraction of the heart muscle and the tense valves, 
and the "dup" being chiefly caused by the slapping to of the aortic 
valves. After listening in this region we next place the ear over the 
second right costal cartilage, in order to come as near as possible to 
the point of greatest intensity of the sound, produced by the aortic 
valves. If the heart is normal, we find only these sounds, "lub dup," 
and nothing else. If it is feeble from exhausting disease, from faint- 
ing, or by reason of fatty degeneration, we find that the sound "lub" 
is feeble, and the "dub" sound is also feeble, because the valves do 



AUSCULTATION OF THE HEART AND VESSELS 



24." 



not slap hack into place with as much force as is normal. If, on the 
other hand, the heart is bypertrophied or stimulated, we find these 
.sounds accentuated, and it is of importance to remember that marked 
accentuation of the aortic second sound, showing forcible closure of 
the aortic valves, indicates a condition of high arterial pressure, 
often the result of vascular spasm arising from chronic contracted 
kidney or general arterial sclerosis. On the other hand, if the pul- 
monary second sound at the third left intercostal space is accentuated, 
it indicates an increase in pulmonary pressure due to impediment to 
the flow of blood in the lungs. This pulmonary second sound is 




Fig. 92. — Approximate positions of the valves of the heart To the lelt the mitral, in the 
centre the pulmonary, to the right the tricuspid, uppermost the aortic. Com] tare with this 
the figure Showing where the sounds of these valves are actually best heard (Fig. 91). 

markedly accentuated in both mitral obstruction and regurgitation 
and in some cases of pneumonia and emphysema. 1 

The sound produced at the various orifices of the heart are heard 
best at or near the following points (Fig. 91), although the approxi- 
mate positions of the valves are shown in Fig. 92. The mitral valve is 
heard best at the apex beat; the aortic valve at the second right 
costal cartilage, the tricuspid valve over the sternum on a line drawn 
from the third left intercostal space to the fifth right costal cartilage, 
and the pulmonary valve at the third left intercostal space. All the 
heart sounds may be reduplicated in health and in disease. When 



i By accentuation, I do not mean necessarily any increase in the loudness or volume of the 
sound, but au increase in its sharpness. 



24(3 THE THORAX AND ITS VISCERA 

the first sound is reduplicated, it probably is due to asynchronism of 
the ventricles, and when the second sound is doubled there is asyn- 
chronous tension of the two sets of sigmoid valves. If disease of 
the valves be present, we are apt to find reduplication of the second 
sound in cases of mitral stenosis and in pulmonary disease producing 
an abnormally high tension in the pulmonary circulation. Such 
reduplication is also seen in some individuals suffering from aortic 
stenosis. 

The Significance of Heart Murmurs.— Supposing that on listen- 
ing to the heart in the mitral area — that is, in the neighborhood of 
the apex beat — there is heard in place of the normal sounds ("lub 
dup"), or with them, a murmur. What does it mean? It means 
that, friction sounds being excluded, either valvular disease, a relaxed 
mitral orifice, aneurysm of the aorta, or marked anemia is present. 
Still more rarely the sound may be due to what is called a cardio- 
pulmonary murmur, which may occur at any time in the cardiac 
cycle. This sound is produced not by the movement of the lung in 
the respiratory act, but by the movement of the lung by the action of 
the heart, a movement which occurs approximately seventy times a 
minute, instead of fourteen times, as it would if respiratory. The 
sound is produced, not in the heart, but by the displacement of air 
in the lung, and the murmur can often be arrested or altered in char- 
acter by changing the posture of the patient. The absence of any 
signs of cardiac difficulty, such as are met in true cardiac disease, and 
the fact that holding the breath on expiration or inspiration may stop 
the murmur, aid us in suspecting that the murmur is one of the cardio- 
pulmonary type, particularly as it is apt to be musical in character. 

The anemic murmur is particularly apt to be heard in the case 
of a feeble child suffering from chorea, or, if in an adult, in associa- 
tion with other signs of disorder of the blood, which should make 
the physician suspect this condition to be the cause. Further than 
this, an anemic murmur is apt to be soft and purring, and associated 
with rather feeble heart sounds, probably due to the fact that the 
heart muscle is not well nourished; such a murmur will generally 
be found most marked at the left margin of the sternum near the 
third interspace. 1 (See chapter on Blood for illustration.) 

Having found that there is a murmur, and having excluded the 
causes just named, it is now necessary to determine at what orifice 
of the heart it is produced, and the rule is to be remembered that a 
murmur is nearly always heard loudest at about its point of origin. 
We therefore place the ear over the aortic cartilage (second right). 
If the murmur be mitral in origin, it will not be heard at this place, 
unless it be so loud as to be transmitted from the apex. If it is aortic 

i It must not be forgotten that murmurs due to endocarditis also are frequently found in 
choreic children. 



AUSCULTATION OF THE UK ART AND VESSELS 



247 



in origin, it will he louder here than at the apex. If it is tricuspid, 
it will be loudest in the tricuspid area; if pulmonary, loudest at the 
pulmonary area (Fig. 91). As murmurs at the tricuspid and pulmon- 
ary valves are rare, we nearly always have to deal with aortic or mitral 
murmurs, or both. In this way, therefore, we can determine the 
origin of the murmur, and that it is a mitral or an aortic murmur. 

Mitral Murmurs. — Let us suppose that it is mitral. We must 
determine whether it is that of mitral regurgitation or obstruction, 
or, as they are also called, incompetence and stenosis. 




Fig. 93. — Diagram modified from Page to show the relation of the various valves. A study 
of this diagram will render clear the time of the various cardiac murmurs. Thus in mitral 
regurgitation the blood passes back from the left ventricle to the left auricle during systole, 
and is dammed up in the pulmonary veins, the openings of which are seen in the auricular 
wall, producing pressure on the pulmonary valves, the sound of which is thereby accent- 
uated. 

The probabilities are that it is the mitral regurgitation, because 
this is by far the most common murmur heard in the heart; and if 
to this probability we add the fact that it is transmitted well into the 
axilla, and even heard at the angle of the scapula, our diagnosis 
is greatly aided, for this is the area of transmission of the murmur 
of mitral regurgitation (Fig. 94). The most important diagnostic 
point, however, is the discovery that the murmur occurs simultane- 
ously with the first sound of the heart, or with systole— that is, with 
the apex beat or the carotid pulse. If it does, and the other signs of 
mitral disease are present, it is almost certainly one of mitral regurgi- 



248 THE THORAX AND ITS VISCERA 

tation. This murmur occurs with the first sound, or systole, because 
the ventricle in contracting drives most of the blood in the normal 
direction into the aorta, and also forces some of it back through the 
left auriculoventricular orifice into the auricle, causing a regurgitant 
murmur. (See Fig. 93.) Sometimes there will be found in such cases 
a very marked accentuation of the second sound at the pulmonary 
orifice, due to the increased pressure in the pulmonary veins by 
reason of the blood, which has been dammed back into them by the 
distention of the auricle due to the blood which regurgitates into it. 
The area of greatest intensity of the mitral regurgitant murmur is 
shown in Fig. 94. 




Fig. 94. — Showing at x the apex beat where the murmurs of mitral regurgitation and 
obstruction can be best heard. The arrow pointing to the axilla indicates the direction in 
which the regurgitant murmur is transmitted, and the arrow pointing to the sternum the 
direction of transmission of the obstructive murmur. 

In adults inspection and palpation will rarely reveal much of a 
thrill over the precordium in mitral regurgitation, but in children 
this thrill is rarely absent and is usually well marked. Percussion 
will show that the area of cardiac dulness (see earlier part of this 
chapter) is broadened, extending beyond the right edge of the ster- 
num and to the left of the mammillary line. 

If the pulse is irregular and asynchronous with the heart beats, 
the heart enlarged by dilatation, and the urine scanty, we recognize 
that compensation is lacking and treatment needed. 

In the diagnosis of the mitral regurgitant murmur the physician 
must not be misled by a loud aortic systolic murmur transmitted 
down the sternum to the area of the apex beat. 



AUSCULTATION OF THE HEART AND VESSELS 



240 



If the murmur is due to mitral stenosis, it will he found that 
it does not occur with systole, but just before it, and is not trans- 
mitted into the axilla, but to the right, over to the midsternal 
line, and it is presystolic in point of time (Figs. 94 and 95). This 
murmur can often be exaggerated by placing the patient in a 
prone position, and occurs before systole, or the first sound, because 
it is produced by the blood passing through an obstructed left 
auriculoventricular orifice, and, as the ventricle does not contract 
(systole) until it is filled, the murmur must be made while it is filling, 




Fig. 95. — MO shows area of greatest intensity of a mitral obstructive murmur. TK shows 
area of greatest intensity of a tricuspid regurgitant murmur; both lesions were present in this 
patient. The fine lines indicate the area in which is felt the characteristic thrill of mitral 
stenosis. (From the author's wards.) 

and so is presystolic in time. Palpation of the precordium in such 
a case will usually reveal a marked diastolic thrill in the fourth or 
fifth interspace. If the compensation of the heart in a case of mitral 
stenosis is broken, these signs are accompanied by a very irregular 
action of the heart, the first sound becoming accentuated and the 
murmur disappearing or being inconstant, because the auricle is too 
feeble to drive the blood forcibly through the orifice. In some cases 
what is called a "gallop rhythm" develops, the heart sounds being 
reduplicated in such a manner as to make a sound somewhat resem- 



250 THE THORAX AND ITS VISCERA 

bling that made by a horse's feet when it is galloping. If in addition 
to these physical signs the physician finds cyanosis, jugular disten- 
tion, congestion of the lungs and liver, and dyspnea, indicating a 
failing heart, for the venous system is engorged and the arterial 
system starved, the diagnosis of mitral stenosis with failure of com- 
pensation is established. 

In the diagnosis of mitral obstruction the physician must not be 
misled by the possible presence of what is known as Flint's murmur, 
a presystolic murmur heard in the mitral area, and due to relaxation 
of the mitral valves, which are thrown into vibration during diastole 
by blood regurgitating from the aorta in aortic regurgitation. 

Aortic Murmurs. — If, however, we have found the murmur to be 
aortic in origin, we must determine whether it is that of aortic regurgi- 
tation, aortic roughening, aortic obstruction, or aneurysm. Aortic 
obstruction or roughening is so common that it must be excluded 
from the diagnostic possibilities before any further steps are taken. 

This murmur occurs with the systole of the ventricles, and the 
carotid pulse and apex beat; it is harsh, as a rule, and is transmitted 
up into the carotid, and it may be into other arteries of less impor- 
tance (Fig. 96). It is produced by the contraction of the ventricle 
driving the blood through a narrowed or roughened aorta or 
aortic orifice. A similar murmur may arise from vegetations on the 
aortic valves. Considerable hypertrophy of the left ventricle is 
usually produced, and the apex beat is strong and forcible if com- 
pensatory hypertrophy is present. 

As a matter of clinical fact, true aortic obstruction, due to vege- 
tations on or contractions of the aortic valves themselves, is always 
associated with a certain degree of aortic regurgitation, even though 
the regurgitant murmur may not be discoverable. Aortic systolic 
murmurs entirely free from an aortic regurgitation are really due to 
aortic roughening produced by atheromatous plaques on the aortic 
wall. 

If the murmur occurs after the systole or the apex beat and is 
aortic, the murmur is that of aortic regurgitation, and is called the 
diastolic aortic murmur. It is heard loudly at the aortic cartilage 
(second right) , often equally marked to the left of the sternum, and 
it is transmitted down along the sternum very clearly and into the 
left ventricle, so that it is plainly heard at the apex (Fig. 97). In 
this condition we have usually marked dilatation of the heart with 
hypertrophy (the so-called "ox-heart"), and a peculiar trip-hammer 
pulse (see chapter on Pulse), sometimes called the "water-hammer" 
or Corrigan pulse. This murmur is due to incompetence of the 
aortic valves, which allow the blood to regurgitate into the heart 
after it is driven out into the aorta. If in association with this mur- 
mur we find irregularity of the action of the heart, a lack of sharpness 



WSCl LT VTION OF THE HEART AND VESSELS 



!ol 



in its sounds, displacement of the apex beat downward and to tin- 
left, extension of cardiac dulness to the right, and a feeble pulse, then 
we know that the heart is failing. Finally, a soft mitral systolic mur- 
mur and the development of rales in the chesl at the base of the lungs 
show still greater failure, the result of dilatation of the mitral orifice, 
which is the result of the strain produced at this area by the constant 
regurgitation and consequent dilatation of the left ventricle. The 
objective symptoms of valvular disease are described later on. 





Flu. % — Showing the area of greatest inten- 
sity and the direction of transmission into 
subclavian and carotid arteries of the aortic 
obstructive murmur. 



Fig. 97. — Showing the area in which the 
murmur of aortic regurgitation can be most 
clearly heard. 



Aortic Aneurysm. — The characteristic symptoms of aortic aneu- 
rysm vary greatly with the site of the lesion, as will he pointed out 
below. The most typical signs are a "bruit" or angry murmur, 

systolic in point of time, thrill over the growth, dulness on percussion 
over the area of this thrill, dyspnea, cardiac hypertrophy, and func- 
tional disturbance of the heart. Finally, a history of alcoholism, 
syphilis, and severe strain or injury will be a valuable indication of a 
causative factor. It is to be remembered that small aneurysms deeply 
situated, which do not press upon other organs, may produce no 
symptoms for years, and finally be discovered only at autopsy. When 
the ordinary signs of aneurysm are not clear, an examination of the 
radial pulses may reveal that one of them is delayed, and this is a 
confirmatory sign of aneurysm. ^ 

Although the general symptoms of aortic aneurysm have just been 



252 



THE THORAX AND ITS VISCERA 



described, there are others which depend upon the seat of the aneu- 
rysm, and which materially modify the importance of the points so 
far named in diagnosis. Let us suppose that a patient presents him- 
self with great engorgement of the vessels of the head and neck and 
arm of the right side, with perhaps edema of that arm. The heart 
may be pushed downward and to the left and the voice may be lost 
or partially impaired by pressure on the recurrent laryngeal nerve of 
the right side. The pupil of the eye may be widely dilated through 
irritation of the sympathetic, and there may be unilateral pallor of the 
face from this cause. This influence of the cervical sympathetic has 




Fig. 98. — Case of aortic and innominate aneurysm, with erosion of the clavicle and ribs 
from the author's wards in the Jefferson Medical College Hospital. This case is of extraordi- 
nary interest because this picture was taken thirty-five months after an arrest of the growth 
of the aneurysm by electrolysis. 

recently been denied and the condition is ascribed to syphilis, which 
often causes mydriasis, but this theory does not explain the fact that 
the mydriasis and aortic lesion are on the same side. If the pupil is 
contracted, then the ciliospinal fibers are paralyzed by pressure. In 
such a case pain is apt to be a prominent symptom and so severe as 
to be almost like that of true angina. Percussion over the second 
right interspace will give impaired resonance, and auscultation of 
the area of the pulmonary valve may show a pulmonic systolic mur- 
mur, due to pressure on the pulmonary artery, which in turn causes 
hypertrophy and dilatation of the right ventricle. There may be 



M'SCVLTATIOS OF THE HEART AND VESSELS 



253 



bulging of tlie first, second, or third interspace on the right side. 
Generally such symptoms will be due to an aneurysm of the greater 
curvature of the ascending aorta, although they may be due to a 
tumor in the anterior or middle mediastinum; but the expansile 
pulsation, the bruit, and the history of the case will usually make the 
differentiation possible. 

Again, let us suppose that the patient has a ringing, brassy cough, 
difficulty in swallowing, and expansile pulsation in the episternal 
notch and epiclavicular space of the left side, and dulness on per- 
cussion over the first and second left intercostal spaces. The left side 




Fig. 99.— Pointing of an aneurysm of the descending part of the aorta between the 
vertebra' and shoulder blade. 



of the face and neck may be engorged from pressure on the left 
innominate vein. Pupillary symptoms similar to those already 
named may be present. There is difficulty in breathing, particularly 
on inspiration, owing to the pressure of the growth on the trachea, 
the paralysis of the left vocal cord, and the pressure on the left bron- 
chus, and there is dysphagia due to pressure on the esophagus. The 
voice is altered from paralysis of the vocal cord due to pressure on 
the left recurrent laryngeal nerve. (See Fig. 100.) These symptoms 
indicate a lesion of the transverse arch. 



254 



THE THORAX AND ITS VISCERA 



If, however, none of these important signs are present anteriorly, 
we must search for some of them posteriorly, particularly the bruit 
and the expansile pulsation, and, if these are found to the left of the 
vertebral column opposite the angle of the scapula, we can rest assured 
that the aneurysm involves the descending aorta. Severe intercostal 
pain is often felt in these cases. 

In this connection it is well to recall the fact that aneurysm of the 
ascending portion of the aortic arch is by far the most common con- 
dition. Out of 953 cases of aortic aneurysm, analyzed by myself and 
one of my former assistants, Dr. Holder, no less than 570 were situ- 




Fig. 100. — A posterior view, showing how an aneurysm of the transverse aorta presses on the 
recurrent laryngeal nerve. The cut shows the relation of the aorta, where it is surrounded by 
the loop of the recurrent nerve, to the left bronchus and the lower part of the trachea. 
A, aorta; P, pneumogastric nerve; R, recurrent nerve; L, larynx. (Dieulafoy.) 

ated in the ascending part of the arch; of these, 544 were sacculated 
and 26 fusiform. Aneurysm of the transverse arch occurred 104 
times, and of the descending part 110 times. Of the 544 cases, 
400 were in males. 

There are other symptoms connected with aneurysm which should 
not be overlooked. The first of these is " tracheal tugging," a sign 
which is found in some cases but not in all. The patient being in 
the erect position, the fingers of the physician grasp the cricoid 
cartilage and gentle upward traction is produced. If aneurysm is 
present, a distinct tug will be felt with each beat of the heart. It 



AUSCULTATION OF THE HEART AW) VESSELS 255 

is important for us to remember, however, that this sign of aneu- 
rysm is not pathognomonic, for, as Sewell has pointed out, it may 
occur in patients who have adhesions of the left pleura or diminished 
extensibility of the lung, or both combined. Further, in healthy 
persons the descent of the heart with the diaphragm on deep inspira- 
tion may press the aortic arch on the left bronchus, and so transmit 
to the trachea a tug not due to aneurysm. Another sign emphasized 
by Osier is the loss of pulsation in the peripheral vessels, the result 
of the loss of the heart's impulse in the aneurysmal sac. 

Doubtful cases of aortic aneurysm should be subjected to the use 
of the radiograph and fluorosebpe, since this will often reveal the 
growth, particularly if the sac contains a firm clot. 

Tricuspid Murmurs. — If the examination has shown that the mur- 
mur is loudest in the tricuspid area, it is to be remembered that in 
the vast majority of cases the condition is one of tricuspid regurgi- 
tation, for tricuspid stenosis is an exceedingly rare lesion. The time 
of the murmur of the tricuspid regurgitation is identical with that of 
the mitral regurgitation (systolic), because the tricuspid valves are 
the counterpart in the right side of the heart of the mitral valves in 
the left. (See Fig. 93.) 

This murmur is best heard in Fenwick s triangle, the base of 
which extends two inches to the right of the sternum on the line 
of the sixth chondrosternal articulation, the apex of the triangle 
being at the level of the fourth chondrosternal articulation. (See 
Fig. 95.) 

Pulmonary Valvular Murmurs. — Actual disease of the pulmonary 
valve is exceedingly rare, and usually congenital; pulmonary regurgi- 
tation is almost never met with. The signs of pulmonary stenosis due 
to congenital defect are cyanosis, hypertrophy of the right ventricle, a 
systolic murmur at the left side of the sternum, which is not trans- 
mitted upward, and a weak pulmonary second sound. The murmurs 
sometimes heard, and the thrills sometimes felt, in the pulmonary 
area are generally due to anemia, the puerperal state, or some neu- 
rosis, or to congenital narrowing of the pulmonary artery, or to 
compression of the vessel by the heart. If the last two causes are 
present, the ventricular septum is usually deficient and cyanosis is 
noticeable. 

The following rules, laid down by Hochsinger, may be used for 
making the diagnosis of congenital cardiac disease. 

1. In childhood loud, rough, musical heart murmurs, with normal 
or slight increase in the heart dulness, occur only in congenital heart 
disease. The acquired defects with loud heart murmurs in young 
children are almost always associated with great increase in the 
heart dulness. 

2. In young children heart murmurs, with great increase in the 



256 THE THORAX AND ITS VISCERA 

cardiac dulness to the right and feeble apex beat, suggest congenital 
changes. The dulness to the left is only slightly altered. On the 
other hand, in the acquired endocarditis in children, the left heart 
is chiefly affected and the apex beat is visible; the dilatation of the 
right heart comes late and does not materially change the increased 
strength of the apex beat. 

3. The entire absence of murmurs at the apex, with their evident 
presence in the region of the auricles and over the pulmonary orifice, 
is always an important element in differential diagnosis, and points 
rather to septum defect or pulmonary stenosis than to endocarditis. 

4. An abnormally weak second pulmonic sound associated with 
a distinct systolic murmur is a symptom which, in early childhood, 
is to be explained only by the assumption of a congenital pulmonary 
stenosis, and possesses, therefore, an importance from a point of 
differential diagnosis which is not to be underestimated. 

5. Absence of a palpable thrill, despite loud murmurs which are 
heard over the whole precordial region, is rare, except with con- 
genital defects in the septum, and it speaks therefore against an 
acquired cardiac affection. 

6. Loud, especially vibratory, systolic murmurs, with the point 
of maximum intensity over the upper third of the sternum, associated 
with a lack of marked symptoms of hypertrophy of the left ventricle, 
are very important for the diagnosis of a persistence of the ductus 
Botalli (ductus arteriosus), and cannot be explained by the assump- 
tion of an endocarditis of the aortic valve. 

Associated Murmurs. — In the diagnosis of all murmurs in the heart 
we must remember that several orifices may be diseased, producing 
associated murmurs. Some discussion as to the relative frequency of 
these associations has arisen, but the results of H. J. Smith derived 
from the London hospitals are usually accepted as correct. His 
results are as follows, in the order of frequency and association: 

1. Aortic regurgitation and stenosis and mitral regurgitation. 

2. Mitral stenosis and regurgitation. 

3. Aortic stenosis and mitral regurgitation. 

4. Aortic regurgitation and mitral stenosis. 

5. Aortic regurgitation and stenosis. 

6. Aortic regurgitation and stenosis; mitral stenosis and regurgi- 
tation. 

7. Mitral regurgitation and tricuspid regurgitation. 

8. Aortic regurgitation and stenosis; mitral regurgitation; tri- 
cuspid regurgitation. 

9. Mitral stenosis and regurgitation; tricuspid regurgitation. 

10. Aortic stenosis; mitral stenosis and regurgitation. 

11. Aortic regurgitation; mitral stenosis and regurgitation. 

12. Aortic stenosis; mitral regurgitation; tricuspid regurgitation. 



AUSCULTATION OF THE HEART AND VESSELS 257 

13. Aortic regurgitation and stenosis; mitral regurgitation; pul- 
monary regurgitation. 

14. Aortic stenosis and regurgitation; mitral stenosis. 

15. Aortic regurgitation; mitral stenosis. 

16. Aortic regurgitation; mitral regurgitation; tricuspid regurgi- 
tation. 

17. Mitral stenosis; tricuspid regurgitation. 

IX. Aortic stenosis; mitral stenosis and regurgitation; tricuspid 
regurgitation. 

19. Aortic stenosis; mitral stenosis. 

20. Aortic regurgitation and stenosis; mitral stenosis and tricus- 
pid regurgitation. 

21. Aortic regurgitation; mitral stenosis and regurgitation; tri- 
cuspid regurgitation. 

22. Aortic regurgitation and stenosis; mitral stenosis and regur- 
gitation; tricuspid regurgitation. 

23. Aortic regurgitation and stenosis; mitral stenosis and regur- 
gitation; tricuspid stenosis and regurgitation. 

24. Aortic stenosis; pulmonary stenosis. 

25. Aortic stenosis; mitral stenosis and regurgitation; tricuspid 
stenosis and regurgitation. 

2(). Mitral stenosis and tricuspid stenosis. 

The relative gravity of heart lesions is, according to Walsh, as fol- 
lows, the least dangerous being placed last and the most dangerous 
first: 

Tricuspid regurgitation. 
Mitral obstruction and regurgitation. 
Aortic regurgitation. 
Pulmonary obstruction. 
Aortic obstruction. 
Pericardial Friction Sound is, of course, heard best in the precor- 
dium at the base of the heart — that is, at about the third rib. It is 
separated from pleural friction by its frequency and by the fact that 
it continues when the patient holds his breath. (See Fig. 101.) 

Laennec likened this friction sound to the noise made by the 
leather of a new saddle when used for the first time. Sometimes it 
sounds like the crunching of dry snow under the shoe. It is usually 
a to-and-fro sound. 

General Symptoms of Valvular Disease with Ruptured Compensation. 
— The general symptoms, subjective or objective, which a patient 
suffering from the various forms of valvular lesion presents, in some 
instances, have not been spoken of up to this point, because it is to 
be distinctly understood that murmurs produced by any form of 
valvular lesion may exist with great intensity without there being any 
systemic disturbance or the patient being conscious of their presence. 
17 



258 



THE THORAX AND ITS VISCERA 



On the other hand, the murmur may be so faint as to be almost 
indistinguishable, and yet the general symptoms of heart disease be 
very marked. This is because the development of general symptoms 
depends entirely upon the question of compensation by hypertrophy. 
If there is a leak in a valve or a constriction of an orifice, this leak 
or obstruction must be overcome by compensatory hypertrophy of 
the heart muscle. If the heart muscle can make up for the regurgi- 
tation or Obstruction by increased effort, the circulation is unim- 
paired; but if it cannot do so, we have developed more or less rapidly, 
according to the lesion present and the condition of the heart muscle, 
characteristic symptoms. 




Fig. 1U1. — Area in which pericardial friction sound is best heard. 

Let us suppose that the valvular lesion is that of mitral regurgi- 
tation with failure of compensation. The first and one of the most 
prominent symptoms is shortness of breath on exertion; the lips and 
ears do not possess their normal red hue, but are a little bluish; and 
if the congestion of the auricle and pulmonary veins is great, bron- 
chitis may be constant or attacks of hemoptysis may develop. Pal- 
pation of the heart will also be complained of; and if the patient 
has developed the lesions in early life, the finger tips are apt to be 
clubbed. If the rupture or failure of compensation is more complete, 
all these symptoms become more marked, and the shortness of breath 
even when lying down, becomes most distressing; indeed, the patient 
may be comfortable only when sitting up. Dropsy of the lower 
extremities now comes on; the liver becomes enlarged from portal 



AUSCULTATION OF THE HEART AXD VESSELS 259 

congestion, and this results in disordered gastric digestion by the 
catarrh of the stomach which ensues, while the urine become albu- 
minous, not necessarily from any true renal lesion, but as the result 
of engorgement of the kidneys with blood. 

The general symptoms of mitral obstruction are identical with 
those just described. For the differential physical signs see page 249. 

The general symptoms of aortic obstruction are also much like 
those described as resulting from mitral regurgitation, but in addi- 
tion there are apt to be present, early in the process of failing com- 
pensation, some lightness of the head, dizziness or vertigo, or 
faintness, owing to a deficient blood supply to the brain. Very 
commonly, too, it will be found that in association with the aortic 
stenosis there also exists mitral regurgitation, which speedily pro- 
duces in its turn well-marked pulmonary symptoms. Dropsy is very 
rarely seen in patients with aortic stenosis. On the contrary, they 
present, as a rule, the lean and poorly-nourished appearance so often 
found in the adult, well advanced in years, who has atheromatous 
tendencies in the bloodvessels. 

The association of ruptured compensation with aortic regurgita- 
tion presents more typical general systemic symptoms than any of 
the ordinary valvular lesions of the heart. In addition to headache, 
vertigo, and a tendency to syncope associated with palpitation and a 
sense of cardiac oppression, we often have a great deal of cardiac pain, 
of a dull, aching character in rare instances, but more often intensely 
sharp and lancinating, often darting down the left arm, particularly 
at night. The dyspnea is often extreme, the patient suffering from 
terrible attacks of shortness of breath and often sitting day and night 
in a chair with his head resting on the back of a chair placed in front 
of him. As time gees on the constant struggling for breath exhausts 
him, and he falls asleep, only to wake in a few moments gasping for 
air. Long before any of these grave symptoms arise we may, how- 
ever, find a number of interesting signs of this heart lesion, chief 
among which is the " water-hammer" or "trip-hammer" or "Corri- 
gan pulse," the throbbing arteries, and capillary pulsation in the skin 
and mucous membranes is to be seen. The last is best developed 
by drawing the thumb nail sharply across the forehead, thereby 
causing a red mark, which can be seen paling and flushing with each 
beat of the heart (Quincke's sign), or by pressing a glass slide on the 
inner part of the lower lip, when the same capillary pulsation will 
be found. Ophthalmoscopical examination will often reveal similar 
pulsation of the retinal arteries. 

Dilatation of the Heart. — Beyond valvular lesions we have a 
number of other causes which seriously disturb the action of the 
heart and the general circulatory condition. The first of these is 
dilatation of the heart, independent of associated valvular disease. 



260 THE THORAX AND ITS VISCERA 

Let us suppose that a man presents himself with a history of short- 
ness of breath on exertion, so great that his activities are greatly 
reduced and his usefulness impaired. He gives a history that he 
was well until he made some extraordinary exertion. Since that 
time his symptoms of heart failure have been marked. He may 
perhaps have attacks of syncope. Examination of his heart reveals 
on inspection a diffuse thrill in the region of the apex; but this thrill 
is too feeble to be felt, though well marked to the eye if his chest is 
thin. Percussion shows that the area of cardiac dulness is increased 
vertically and laterally, and auscultation will discover feeble heart 
sounds. If the dilatation of the muscular portion of the heart is 
associated with dilatation of the orifices, a murmur may be present, 
most commonly that of mitral regurgitation, without there being in 
association any actual disease of the mitral valves. Sometimes tri- 
cuspid regurgitation is also found. The first sound, before it becomes 
very feeble, may be short and flapping like the ordinary second 
sound. Marked arhythmia of the heart is often present. 

The influence of severe strain in producing cardiac disease deserves 
careful study on the part of the physician. The study can be divided 
into three parts : The condition of the heart immediately after acute 
overstrain, the condition after chronic overstrain, and the final con- 
dition often met with months or years after the occurrence of the 
strain. 

It is now well known that immediately after severe muscular 
effort an examination of the heart will often reveal in entirely healthy 
persons a distinct increase in the area of cardiac dulness, and, not 
infrequently, a murmur which disappears with rest. The increase 
in the area of dulness is, of course, due to more or less cardiac dilata- 
tion and the murmur to the same causes, since the dilatation results 
in stretching of the circular muscular fibers governing the mitral or 
tricuspid orifices, so that even if the valves be healthy they cannot 
close the orifice (Fig. 102). In some cases this action seems to be 
in the nature of a safety valve, in others a sign that the heart has 
been unduly strained. In the first class the murmur disappears at 
once or very shortly after the exertion ceases; in the other case it 
persists until after a long period of rest, when the heart has had a 
chance to recuperate and regain its normal tone. Persons having 
the latter condition ought to be advised against such forms of exer- 
cise, particularly if they are old in actual years or prematurely aged. 

But the physician who regards physical strain as being the only 
kind of strain which is apt to be productive of grave cardiac damage 
is much astray. It is quite true that sudden cardiac failure due to 
great nervous or mental shock is not uncommon, but such attacks 
being chiefly due to vasomotor relaxation are quickly recovered from. 
On the other hand we meet with hearts which are distinctly 



AUSCULTATION OF THE HEART AND VESSELS 



261 



damaged by prolonged nervous worry. I have met with this most 
frequently in men who have been very successful in business 
or in their professional life, men whose success has been largely due 
to great persistency of effort, who have had great mental strains in 
carrying through some business deal, and have simultaneously used 
a good deal of physical force in long journeys or busy days on foot 
at the same time. Not only do such cases develop the various cardiac 
neuroses, but not rarely such lives seem to bring on the development 
of actual organic and degenerative changes in the heart muscle and 
bloodvessels. That these changes are the result of nerve strain more 
than to infection or exposure is shown by the frequency of these states 
in the officers of great corporations and their infrequency in the 



Aortic valves 



Mitral valve -L 




Pulmonary valves 



Aortic valves 



Tricuspid valves 



Left ventricle 

Right ventricle 
Fig. 102. — The dotted lines show the dimensions to which the heart and its orifices increase 
in diastole, and in pathological dilatation this may be permanent. (Modified from His and 
Spalteholz.) 

employes who perform the manual Labor. There can be no doubt 
that one cause of this lies in the great increase in the heart action 
required by mental effort, accompanied as it is by nervous stress 
without the compensation of long periods of rest, of outdoor exercise, 
and fresh air. Recent studies with instruments of precision have 
shown that increased mental activity causes circulatory activity to a 
greater degree than is generally thought. Such persons run at a 
high tension for years, develop a state of chronic vascular spasm and 
high arterial tension, and break down when the heart finds itself 
tired out with the stress laid upon it. These patients, too, when fail- 
ure of energy first begins to creep upon them, use their will power 
to drive them to greater effort, and often very unwisely use stimu- 
lants to act as a spur to greater effort, 



262 THE THORAX AND ITS VISCERA 

Closely associated with these patients is that class who suffer from 
prolonged feebleness of the heart after an attack of true influenzal 
infection, a feebleness which may last for many years. In many of 
these patients it is most difficult to determine how much the feeble- 
ness of the heart depends upon real changes in its muscular fibers 
and how much upon lack of proper nerve supply to this organ. 
Where there is a history of previous cardiac difficulty there can be 
little doubt that the poison of this disease magnifies it and pro- 
duces far too often a permanent increase in the disease. In 
other instances where the heart is primarily healthy the condition 
is usually a fleeting one, although it is not to be forgotten that 
undue muscular activity on the part of the patient soon after, or 
during, an attack of influenza may be provocative of permanent 
cardiac incompetency. 

What the exact changes in the heart are under these circumstances 
has not, so far as I know, been determined, but during life we cer- 
tainly meet with them clinically. Such patients often suffer from 
faintness and precordial distress on exertion, and physical examina- 
tion usually reveals a feeble and distant first sound, and a second 
sound lacking in tone because of lack of force in the systole of the 
heart. These patients also have edema of the lower extremities, 
sometimes a more or less decided trace of albumin in the urine, but 
no casts unless there be associated renal lesions, the albuminuria 
being due to stasis in the kidney. They are often pallid and relaxed, 
and really need rest and hydro therapeutic measures more than the 
internal use of drugs. Such patients, too, particularly if they are 
advanced in years, not rarely progress rapidly into a gradually 
increasing circulatory feebleness and so to death. 

There is another heart condition closely allied to that just de- 
scribed, at least in one sense, namely, the feeble heart of tuberculosis. 
Too little attention is paid to this organ in this disease, probably 
because the mind is centred upon the lungs. 

Hypertrophy of the Heart. — Again, we have hypertrophy of the 
heart occurring in persons without valvular lesions, sometimes as 
the result of excessive and severe toil. It is seen most commonly by 
the author in medical students, who, during their holidays, devote 
their time to severe athletic sports, or to much manual labor, and 
who, on leading sedentary lives in the winter, develop irregular car- 
diac action, palpitation, and some shortness of breath. Examination 
of the precordium in such cases shows a forcible impulse of the apex 
of the heart against the chest wall, some bulging of the chest wall if 
the hypertrophy be very great, and no murmurs, but in their place 
heart sounds very much louder than normal. Palpation shows the 
apex beat to be lower than normal, and on percussion an increase in 
the area of cardiac dulness is also found. 



AUSCULTATION OF THE HEART AND VESSELS 

Cardiac Neurosis. Again, let us suppose that a patient presents 
himself with the statement that he has attacks in which he suffers 

from a very rapidly beating heart. I lis skin is alternately red and 
pale, and sweats without cause, hut a careful examination of the heart 
fails to reveal any murmurs or organic abnormality. There are con- 
siderable shortness of breath on exertion and marked palpitation and 
arhythmia. Such a case may he suffering from a condition in which 
there is some deficient action of the pneumogastric nerve, whereby 
the heart is not properly controlled, or the irregular cardiac action 
may he due to sudden vasomotor relaxations, which by dilating the 
blood paths reduce the normal arterial resistance. See chapter on 
Blood Pressure and Pulse.) This i- a condition seen in association 
with some neuroses and vers' commonly met with in persons who 
use tobacco to excess. The symptom- of the so-called "tobacco 
heart" are indeed chiefly those of arhythmia due to pneumogastric 
disorder. 

Bradycardia. — Rarely because of irritation of the vagus nerves or 
centres a state of bradycardia develops, in which the heart beat- very 
slowly, perhaps only thirty or even as slowly as twelve time- a minute. 
Bradycardia, or great slowness of the heart, may be due to a neurosis 
of the vagi, and also occurs in some infection- diseases. It i- also 
seen in jaundice. 

Stokes-Adams Disease. — "When a patient suffers from attacks of 
extremely slow pulse with vertigo, syncope, apoplectiform or epilep- 
tiform seizures, associated with pulsation of the veins of the neck 
which are often far more frequent per minute than the beat of the 
ventricle, the condition is called the "Stoke— Adam- syndrome." 
This incoordination of the auricles and ventricles is due to disease 
of the auriculoventricular muscle bundle of His. Graphic tracings 
of the apex beat, the auricular beat, and the jugular beat may 1 e 
made by the use of the multiple sphygmocardiograph of Jacquet. 
(See Fig. 108.) A lever of this instrument work- as doc- the ordinary 
sphygmograph of Dudgeon, the other two by column- of air in 
tubes connected with tambours which are placed on the chest wall. 
(See chapter on Pulse). 

Tachycardia. — One of the most common cause- of tachycardia, or 
rapid heart, is exophthalmic goitre, in which condition we have not 
only exophthalmos and enlargement of the thyroid gland, but, in 
addition to the tachycardia, a marked thrill over the carotid arteries, 
in which vessels a purring murmur of considerable intensity can often 
be heard. The patient often suffers from considerable nervous 
excitement or mental depression. 

An exceedingly irregular arhythmical action of the heart coming 
on in the course of an acute infectious disease, or in any state pro- 
ductive of sepsis, points to the possibility of the patient having an 



2G4 THE THORAX AND ITS VISCERA 

embolism or thombosis of one of the coronary arteries. If the vessel 
is suddenly plugged, death occurs; but if the process is gradual, an 
anemic and feeble necrosis or white infarct is produced. 

Fatty and Feeble Heart. — Before discussing the signs of so-called 
fatty heart we must decide what is meant by this term. True fatty 
heart — that is, that condition of the heart in which this organ has 
undergone true fatty degeneration — has no pathognomonic signs, so 
far as the heart itself is concerned. In these instances we base our 
diagnosis upon the presence of fatty degeneration of the more 
superficial organs, such as the arcus senilis in the eye, 1 the presence 
of atheromatous bloodvessels, the feeble heart sounds at all times, 
and the evident feebleness of the heart on exertion. The history 
of poisoning by any one of the poisons causing fatty degeneration is 
also to be sought after in some cases. Marked fatty degeneration 
is often present in cases of pernicious anemia. It is not possible to 
make a differential diagnosis from the physical signs between fatty 
and fibroid heart. 

Another state quite distinct from true fatty heart, but with some- 
what similar symptoms, is seen in cases in which an excessive 
amount of fat has been deposited around the heart and between its 
fibres as well as in or around the other organs of the body. Here 
there is little or nothing the matter with the heart muscle, except 
that it is overloaded with a weight of fat. 

When a man shows signs of general degenerative changes, has a 
feeble heart, some dyspnea, and perhaps some edema of the lower 
extremities, we may conclude that he has, unless valvular disease 
is discovered, degenerative myocarditis. Valvular disease may, of 
course, be found associated with the myocardial lesion. Such cases 
make up the greater number of sudden deaths, called popularly 
" death by sudden cardiac failure." 

Great feebleness of the heart and of the general system, loss of 
flesh (or sometimes maintenance of weight), and pigmentation of 
the skin and buccal mucous membranes point strongly to Addison's 
disease. (See chapter on the Skin.) 

Sudden attacks of cardiac feebleness sometimes come on as 
cardiac crises in locomotor ataxia and in glossolabiopharyngeal 
paralysis. 

i Ophthalmologists and many clinicians deny that arcus senilis has any significance of this 
character. (See chapter on the Eye.) 



CHAPTER VIII. 

THE PULSE AM) BLOODVESSELS. 

Feeling arid counting the pulse — The condition of the bloodvessels on pal- 
pation — The quality, force, tension and volume of the pulse in health and 

disease. 

One of the first things that the physician does when he is studying 
the condition of a patient is to feel the pulse, even if the symptoms 
which are present do not indicate circulatory disturbance, because 
the pulse is an index of the condition of the heart as to its power. 
its valvular action, and its nervous state. The pulse very often gives 
information of the presence of renal disease, and it will frequently 
give a general idea of the tone or degree of debility of the patient. 
By feeling the pulse we also gather valuable information as to the 
condition of the arteries, and this is a very important part of the 
diagnosis, for, to use an old saying, "A man is only as old as his 
arteries;" and if he is sixty years of age and has good vessels, he is, 
as a rule, younger in health than another man of thirty with had 
vessels, because it is by the bloodvessels that the tissues of the body 
are nourished, and, as life depends upon this process of nutrition, 
the better the vessels the better the vitality. 

When examining the pulse of a patient who is well enough to be 
up and about, the physician should wait until sufficient time has 
elapsed after exercise for the pulse to become steady, and the patient 
should be in a sitting or reclining posture in order to prevent over- 
action of the heart. This is particularly important in the case of ner- 
vous individuals. An entirely erroneous conception of the circu- 
latory state may be reached if this precaution is ignored, and it is 
well to insist on perfect rest in bed for several hours prior to the 
examination in grave cases. 

Often when called to see a sick child or a nervous woman, who 
may be sleeping at the moment of the physician's arrival, a true 
estimate of the pulse can be made without disturbing the patient by 
gently putting the tip of the finger on the temporal artery where it 
passes over the zygomatic process. This fact is of considerable 
importance, because in some patients the excitement of the doctor's 
visit may produce marked alterations in pulse rate. This artery may 
also be used for this purpose in cases of tremor, chorea, delirium, or 
mania, in which the hand is constantlv moved about so that the 
radial artery cannot be felt. 



266 THE PULSE AND BLOODVESSELS 

In counting the pulse it is best to count it for the entire minute, 
or to count it for fifteen seconds and then multiply the result by four. 
If the pulse is irregular, it is always best to count it for a minute. 
If the pulse is very irregular and running, and so difficult of count- 
ing, the estimate should be made by listening at the precordium for 
the apex beat. 

Before considering the significance of arterial changes and the 
qualities of the pulse in health or disease, it is well to understand what 
these are due to and the manner in which the circulation is carried 
on. The bloodvessels consist of the arteries, arterioles, capillaries, 
venules, and veins. These vessels all contain blood during life, and 
the function of the heart is to propel the blood through them. The 
flow of blood is maintained, first, by the force expended by the heart, 
and, second, by the elasticity of the bloodvessels. If the bloodvessels 
of the body become relaxed, as in death, all the blood is readily held 
by the ones most relaxed, namely, the abdominal, thoracic, and other 
veins. We find, therefore, that the vessels are only filled with blood 
when their walls are to a certain extent constricted by the'contraction 
of their muscular and elastic fibers; and that this contraction is 
maintained by the action of the vasomotor centre in the medulla 
oblongata, which also controls many minor centres governing small 
areas of vessels. 

The arteries are very elastic in health, and when filled with blood 
are slightly distended. Behind the column of blood, which being a 
fluid confined laterally is practically a solid, for fluids are incom- 
pressible, is the heart, and in the arterioles are circular muscular 
fibers, which by their contraction regulate the flow of blood into the 
capillaries, from which the nutritional processes are carried on. The 
blood in the arteries is, therefore, subject to three chief pressures, 
namely, that of the heart behind the column, that of the elastic and 
muscular arterial walls on the sides of the column, and the resistance 
of the contracted arterioles in front of the column. By these means 
blood pressure or tension is maintained. If the heart beats more 
strongly or the arterioles contract more tightly than normal, the 
blood stream is under a greater pressure than before. If the heart 
is feeble or the arterioles lax, the pressure falls, because the blood is 
not pressed upon behind or obstructed in its flow in front. If the 
tension is above or below normal, the interchange of food and 
oxygen and carbonic acid between the tissues and the blood in the 
capillaries is perverted, for the rate of flow in the capillaries depends 
largely upon the blood pressure in the arteries. As the capacity of 
the capillary system of vessels is many times greater than that of 
the arteries, if the arterioles relax, the capillaries and veins will 
retain all the blood and it will stagnate and become useless. 

The individual pulse beat is not the wave of blood sent out by the 



TEMPORARY HIGH TENSION 207 

heart, but it is the transmission of the force of the heart beat sent 
along the blood column, and t the character of the beat gives us, 
therefore, an idea of how forcibly the heart is driving another quantity 
of blood into the aorta, and also how much blood is being sent out at 
each beat. 

Supposing, therefore, that on feeling the radial pulse we find that 
the artery is tense and hard, and that the individual beat is strong 
and its volume great; this signifies that there is an excited vasomotor 
centre, causing contraction of the vessels, and that an excited, over- 
acting heart is forcing the blood into the already tense vessels. 

Arterial Tension in Health and Disease.— One of the most 
important acts of the physician is to make a skilful determina- 
tion of the arterial pressure of his patient, since this is of even 
greater importance than the study of the pulse rate. Years of ex- 
perience enable the physician to determine the tension of the arteries 
by his finger tips, and often the degree of tension gives him far 
more information than any other physical sign presented by the 
patient. 

When we come to the study of abnormal arterial tension we find 
that we have to consider cases in which the tension is too high and 
others in which it is too low. 

Temporary High Tension. — 'Faking up cases of high tension first 
we find that we can consider it as normal and pathological. The 
normal cases are those in which the tension is raised to a point 
above normal by exercise or excitement, such tension being a 
natural or physiological response. This form of high tension 
possesses no interest for the clinician unless it is associated with 
the presence of a weak heart or is so great and prolonged that 
it produces cardiac distress or injury. It is the form of high 
tension that frequently damages the heart of the sedentary man 
who suddenly decides that he needs exercise and takes it in 
strenuous and excessive degree. Another type of normal high ten- 
sion, in one sense of the word, is met with in the stage of onset of 
acute febrile diseases when it may be an effort on the part of the body 
to supply more blood to ce tain areas for protective purposes, for all 
large capillary networks are poison destroyers. Still another normal 
or beneficial type of high tension is the high tension of intracranial 
injury or disease, in which states dishing has shown us that the rise 
is essential to the preservation of life. In early CO. poisoning the 
rise of tension is designed to send more blood to the respiratory 
centre, and the rise due to severe pain, as in renal colic, lead colic, 
and labor, may all be advantageous. In the latter case (labor) I have 
elsewhere pointed out that it is this rise of tension produced by pain 
that permits women in labor to take chloroform with relative impun- 
ity. These facts should make us cautious in the use of vascular 



268 THE PULSE AND .BLOODVESSELS 

relaxants, unless we are certain that the high tension is useless 
and actually harmful. If Cushing is right, how many persons have 
been hurried to their end by bleeding in apoplexy. 

Prolonged High Tension. — Aside from those types of high ten- 
sion which are solely due to increased functional activity of the 
vasomotor and vascular systems, there is the high tension of the 
persistent type which often tells of the habits of the patient in 
the past and present, and directs us to the study of his heart, his 
kidneys, and his retinal vessels in a way that must not be ignored. 
In some instances there can be no doubt that a large part of the 
hypertension is functional in the sense that it is not entirely due 
to actual organic changes in the vessels; in other instances it is 
almost entirely due to the presence Of fibroid change and the 
ability of a strong heart to pump vigorously. In some the spasm 
is due to great nervous strain and the use of stimulants, in others 
it is due to poisons in the blood, and in the functional type the 
very existence of these factors for long periods of time results in 
actual lesions. Brunton has recently advanced the view that not 
only does high arterial tension do harm by interfering with the nutri- 
tion of the tissues, but also by interfering with the nutrition of the 
vessels themselves. Thus he points out in his usual lucid way that 
the high tension compresses the vasovasorum between the inner 
coats and the fibrous coat, which is fixed, because it has reached the 
point of fixation by distention. Again, he advances the view that 
the normal constant expansion and contraction of vessels in 
health, like massage, maintains and aids the blood flow in the 
vasovasorum. 

What is the significance of high tension as to the heart? If its 
sounds are approximately normal we learn that it is still a fairly 
healthy organ, able to stand up to its work, but we must bear in mind 
that in many men past middle life a state of increased tension exists 
which is not appreciated because the heart has gradually become 
accustomed to the strain. The stress and strength are so nearly 
balanced that when a sudden increase in exertion is made, as in run- 
ning for a car, or taking any form of violent exercise, dilatation due 
to overstrain at once develops. Abnormal increase in tension means 
increased work for the heart muscle, and increased strain upon its 
valves, particularly the aortic and mitral leaflets. The result of this 
strain is speedily manifested in a previously normal heart by hyper- 
trophy with associated dilatation, in a previously feeble or diseased 
heart by dilatation with increase in its feebleness, in failure of the 
mitral valves to stand the great pressure brought to bear on them 
with each systole, a failure increased in effect by the fact that the 
mitral rim is feeble also, so that mitral regurgitation takes place, the 
result being that the blood finds it as easy to slip back into the auricle 



LOW TENSION 269 

as to pass out into the aorta. The mere high tension due to narrow- 
ing of the arterioles is not alone responsible for this cardiac dis- 
aster; the very fixation of the vessels increases the work of the heart, 
and with fixation come elongation and tortuosity, which demand 
increased cardiac effort. The heart now fails not alone from over- 
work, hut in addition it may begin to develop degenerative changes 
in its fibers, for the same factors that act deleteriously on the mus- 
cular fiber of the vessel wall also act on the more specialized muscular 
fibers of this organ. 

Another question of importance is whether an abnormally constant 
high tension is always evil and ought always to be reduced. Are we 
to regard it as an evil to be attacked, or recognize that it has become 
a necessary and unavoidable evil? The present attitude of the pro- 
fession in regard to high tension is tending to the abuse of vascular 
relaxants in many cases for the following reasons: It is a question 
whether high tension may not be designed by Nature to drive blood 
through narrowed vessels to distant parts for their proper nutrition. 
If we lower pressure by relaxants of the larger arterioles and arteries 
we starve distant tissues. Again, the heart in many eases of high 
tension has undergone compensatory hypertrophy, and this increased 
power and the high tension help to feed the heart muscle itself 
through the coronary vessels and the vessels of Thebesius. Again, 
the normal heart is designed to beat against a pressure of from 
100 to 140 mm. of mercury, and nothing exhausts a heart so 
rapidly as to beat excessively because of low pressure. Very often 
the hypertrophied heart of high tension may be considered to have 
established for itself a new standard of pressure, say of 1 ">() to 170, 
and if this is reduced a state is developed which may be considered 
as abnormal as is a pressure below the true normal. In other words, 
in studying high pressure, it is not sufficient to study the pressure 
alone. We must study the whole cardiovascular apparatus. We 
must endeavor to prevent an increase in tension, but we must not 
reduce tension simply because it is high unless we find that the heart 
cannot stand the stress, or that the pressure is so high and vessels so 
fragile that rupture is threatened. 

Low Tension. — Having considered some of the facts which con- 
cern hypertension in the arterial system, we have still before us the 
study of hypotension. Such a condition, as a chronic state, is rare 
as compared to hypertension, and is most frequently met with as 
a part of some suddenly developed condition in the course of an 
acute illness, or as a result of accident. 

When the hypotension is chronic it depends, in the great majority 
of instances, upon feebleness of the heart muscle, but in one particu- 
lar malady at least we have a persistent low tension not so much as a 
result of cardiac feebleness as of vascular relexation, namely, exoph- 



270 THE PULSE AND BLOODVESSELS 

thalmic goitre, in which disease the thyroid secretion acts as a power- 
ful vascular sedative. 

Not rarely in neurasthenic persons, or persons who are suffering 
from the after-effects of an acute illness, hypotension is an important 
factor. Thus, persistent diurnal somnolence may exist while the 
patient is up and about, replaced by marked nocturnal wakefulness 
as soon as he lies down. This state is due to a low tension which 
prevents an adequate supply of blood to the brain, which organ 
immediately becomes active as soon as the recumbent posture is 
assumed. 

But after all the state of hypotension is met with most frequently 
in acute illness, and it is usually of far greater gravity, when it is 
marked, than is hypertension, because it indicates lack of power, 
nervous and circulatory, and because we have no remedies upon 
which we can rely as all-powerful vascular stimulants as we can 
rely on the nitrites as all-powerful relaxants. 

This condition of hypotension in acute illness may be considered 
under two headings : The first type is met with at the critical period 
of acute infections, of which the most noteworthy is, perhaps, 
croupous pneumonia. It is not uncommon to find in these patients 
at this time a state bordering on collapse: the face is anxious, the 
forehead, wrists, and the trunk bedewed with sweat, the pulse very 
full, but the arteries relaxed, and the heart's action excessive, as it 
actively endeavors to fill the leaking vessels, which do not offer the 
normal resistance to its action. This state depends chiefly, if not 
entirely, upon vascular hypotonus. The second type is met with 
in the course of prolonged fevers, such as typhoid fever, in which 
partly from toxemia and partly from lowered nervous force the 
vessels relax. 

The Estimation of Arterial Tension. — Efforts have been made by 
numerous investigators to devise apparatus which would be capable 
of indicating the condition of arterial tension, but all of them have 
been more or less unsatisfactory. Probably the best at present is 
Stanton's modification of the sphygmomanometer of Riva-Rocci, 
which is well described in Fig. 103. 

In applying the apparatus it is essential that the muscles of the arm 
shall be relaxed, and for this reason the limb should be supported in 
an easy position. Usually it is best to have the patient recumbent 
and to use the left arm as the manipulations by the physician are 
more easily carried out by the right hand. The cuff and armlet 
(F in Fig. 103) are applied together, the ends of the rubber being 
smoothly overlapped. The straps are now buckled, the cuff fitting 
snugly but without compression. 

Before connecting with the manometer the latter should be placed 
on a firm, level surface and the mercury should stand at zero on the 



THE ESTIMATION OF ARTERIAL TENSION 



271 



scale. This is readily accomplished by placing the scale up or down 
on the glass tube. The connection having been made, the valve H is 
screwed tight and the valve A opened (arm parallel to the horizontal 
arm of the T). With the finger of the left hand on the pulse the right 
hand works the syringe. Compression of the bulb forces air into the 
closed system — distending the rubber armlet and with the same 




Fig. 103. — The systolic pressure is determined by noting the point at which the pulse reap- 
pears alter obliteration, while the diastolic pressure is estimated by recording the point at 
which the greatest oscillations occur in the mercury column of the manometer. The pressure lfi 
applied to the arm by a ru» ber armlet which is 10 cm. wide. This armlet is prevented from ex- 
panding outward by a cuff /"of double thick canvass with inserted strips of tin, which is held 
in place by two straps which completely encircle the cuff. On the rigidity of this depends, 
lO a large extent, the transmission of pulsation. The rubber armlet is connected with a stiff- 
walled rubber tube G, which in turn connects with the manometer. The chamber C com- 
municates by means of a metal tube with the glass column D, which is connected by a screw 
thread at 3, the caliber of C being approximately 100 times that of D. The cap of the chamber 
which screws on is provided with a metal T, which is connected at 2 with the rubber armlet 
and at 1 with the bulb used as an air pump. At A is a stopcock shutting the rubber bulb 
completely from the rest of the apparatus, while at B is a screw valve which allows the air to 
escape from the closed system. When desired the manometer can be made portable (without 
removing the mercury) by screwing the caps 1 and 2 into either end of the Tat 1 and 2 Then 
tilt the manometer away from the glass column D until all the mercury has run into the 
chamber: unscrew the glass and screw in cap 3. Before removing cap 3 the manometer must 
always be tilted, else the mercury will be lost. Pressure is established in the apparatus by a 
double bulb syringe similar to those used with the thermocautery. 



degree of force, displacing the mercury in (\ driving it up the glass 
column D. When the pulse is no longer felt, the arm of the valve .1 
is turned until it is at right angles with the thumb and finger. The 
valve B is now slowly unscrewed until the mercury column begins 
to fall. With the eye on the scale, the point at which the pulse reap- 
pears is mentally noted as the systolic pressure. Any pulsation noted 



272 THE PULSE AND BLOODVESSELS 

in the mercury column before the pulse beat reappears at the wrist 
is to be disregarded. As the mercury column falls the oscillations in 
the mercury increase in size until they reach a maximum and then 
decrease. The base line of the greatest oscillation (the line from 
which it starts) is the diastolic pressure. 

Stanton emphasizes the necessity of regarding the following points 
with care : 

In nearly all cases the first estimation will be found 10 to 20 mm. 
higher than subsequent estimations. This is probably due to excite- 
ment arising from fear that the examination will cause pain. Se . eral 
estimations should be made until the level normal to the individual 
is obtained. 

In cases with a very rapid pulse rate the diastolic pressure is hard 
to determine because of the inertia of the mercury. Repeated obser- 
vations may be necessary. 

With a very slow, strong pulse the oscillations may be so large 
that it is hard to distinguish the largest ones. In these cases by leav- 
ing the valve A open some of the oscillation is absorbed by the elastic 
rubber bulb and the reading becomes easier. 

In cases showing threatened circulatory failure, especially in cases 
of high pressure, it will be found almost impossible to get a clear-cut 
high or low pressure. That is, in spite of repeated estimations, the 
high pressures will vary from 5 to 15 mm. These cases may at 
times show a condition in which an occasional beat comes through 
at a much higher level than all the beats can be detected. Often this 
is due to the action of respiration. This should be noted in the 
estimation thus: High pressure, occasional beat at 170; all other 
beats at 155. 

Where the diastolic level is hard to obtain it is of help to get the 
greatest oscillation with increasing pressure as well as with decreasing 
pressure. With the valve A at right angles (shut off from the syringe) 
blow up the syringe until a good pressure is established in the second 
bulb. Now open A very slowly and the air can be made to enter at 
any desired rate of speed. As the mercury column rises the oscilla- 
tions begin, and gradually increase in size until the maximum, and 
then diminish. By shutting off A completely the behavior of the 
oscillations under diminishing pressure can be noted. 

Where it is desirable to compare the point at which the pulse dis- 
appears with the point at which it reappears this can readily be 
accomplished as follows: Inflate the apparatus until the pulse is 
nearly gone, then, dropping the syringe portion, gently compress the 
second bulb until the pulse completely disappears; relaxing the bulb 
allows it to reappear. The normal arterial pressure is recorded 
by the sphygmomanometer varies, of course, with age and disease. 
In normal youths at rest the diastolic pressure is about 100 and the 



THE PULSE 273 

systolic pressure 130 mm. of mercury. In older persons the systolic 
pressure is 100 to 145 and in children from 90 to 110. Excitement 
may raise the pressure, particularly the systolic pressure, as much as 
40 mm., but the error in estimating the pressure produced by thick- 
ened vessel walls can be ignored, as it represents only 5 to 10 mm. 

The fallacies underlying the use of this apparatus are the facts that 
it is only approximately accurate even in well-trained hands and that 
the interest and excitement of the patient, who watches its application 
and often fears the result, sends his tension to an abnormally high 
point which does not represent by many millimeters of mercury the 
real state of the arterial pressure. On the other hand it gives the 
physician a standard which he can use to control the estimates which 
he makes with his finger tips and one of which he can have a record 
in his case-hook and so compare the pressure from time to time. 

The Pulse. — The pulse itself varies as to volume, character, 
rapidity, and force, and does so within normal limits, and still more 
so under the effects of disease. It varies greatly according to age. 
Thus, the pulse of the newborn child is usually about 135 to 1 10, 
at one year 120 to 130, at two years 105, at four years 07, at ten 
years about 90, at fifteen 78, and from twenty to fifty years about 
70 per minute. At eighty years of age it is usually about NO beats 
per minute. The rate is also increased by taking food, by exercise, 
by nervousness, and by pain and fever, as will be stated again 
later. 

The volume of the pulse wave depends chiefly upon the quantity 
of blood expelled from the heart at each systole, and also upon the 
condition of the aortic valves of the heart, in so far as their ability 
to prevent regurgitation is concerned. The stimulation of the vagus 
nerves usually results in a large pulse wave, as does also cardiac 
hypertrophy with dilatation. If, on the other hand, part of the 
blood thrown out of the heart into the aorta falls back into the ven- 
tricle, we have a pulse of small actual volume, and this is called, 
because of the peculiar sensation which it gives to the finger, "trip- 
hammer," "water-hammer," or " Corrigan's pulse." In such a case, 
because of the power of the ventricle, the blood is forced out into the 
aorta with great force, but as the last part of the wave regurgitates 
the pulse is found to be short and sharp. In mitral regurgitation or 
in mitral stenosis the pulse is usually small in volume, because the 
left ventricle has not, or cannot get, enough blood at each beat to 
send out a voluminous wave. (See Figs. 105 and 106.) 

So far as the character of the pulse is concerned, we recognize one 
which is slow and full, as that seen after digitalis is used; that which 
is short and sharp, as in aortic regurgitation; that which is small and 
hard, as is often seen in aortic obstruction, and the small, wiry pulse 
of acute peritonitis. 
IS 



274 



THE PULSE AND BLOODVESSELS 



Various names are applied to a pulse possessing certain peculiari- 
ties. Thus, we have under the name pulsus paradoxus a pulse which 
disappears with each deep inspiration. It is usually due to indura- 
tive mediastinopericarditis, whereby inflammatory bands press on 
the bloodvessels or the heart or suction ensues when large vessels 
are drawn upon. If the beats of the heart are irregular in force but 
regular in rhythm, we have developed what is called a pulsus alter ans. 

A dicrotic pulse is one which is characterized by a reduplication, 
which feels like a second beat following the first before the latter 
is over. It is found in many cases of exhausting fever, and depends 
upon an undue elasticity of the bloodvessels, with relaxation of the 




Fig. 104. — A sphygmograph. Certain supporting parts are omitted so that the multiplying 
levers may be displayed, a is a small metal plate wnich is kept pressed on the artery by the 
spring b. The vertical movements of a cause to-and-fro movements of the lever c about the 
fixed point d. These are communicated to and magnified by the lever e, which moves around 
the fixed point f. The free end of this lever carries a light steel marker which rests on a 
strip of smoked paper, g. The paper is placed beneath two small wheels and rests on a roller 
which can be rotated by means of clock-work contained in the box h. The paper is thus 
caused to travel at a uniform rate. The screw graduated in ounces (Troy) is brought to bear 
on the spring 6 by means of a cam, and by this the pressure put on the artery can be regu- 
lated. The levers magnify the pulse movements fifty times. (Dudgeon.) 

arterioles, so that the blood first unduly distends the arteries, which 
then contract upon it, and thus produce the second wave or apex to 
the pulse curve. 

We can study the pulse either by the touch or by the sphygmo- 
graph. If by the latter means, the instrument of Dudgeon is the 
best (Fig. 104). The normal pulse wave is shown in Fig. 105. 

It will be seen that there is a distinct upstroke produced, which is 
called the line of ascent. This is due to the distention of the artery 
produced by the ventricle forcing blood out into the aorta. There 
is after this a line of descent interrupted by two separate secondary 



THE PUS 



275 



waves, which are called catacrotic waves. The second or lower of 
these is cjdled the dicrotic wave, and is the one which becomes marked 
enough to he felt in some cases of disease. The duration of the 
period of descent corresponds to the time the blood is flowing out of 
the arteries into the capillaries, and, if this flow is rendered difficult 
•by vascular spasm, the line of descent will be gradual; if easy from 
vascular relaxation, it will be short. If the drop is very sudden, it is 
a pulse of "empty arteries," SO called, as after severe hemorrhage 
or in cases of aortic regurgitation. 




Fia. 105.— a b. Percussion upstroke, a b c. Percussion wave, r H e. Tidal wave. 
e f g. Dicrotic wave, d e f. Aortic notch, f g. Diastolic period. 

Very small irregularities of the line of descent are due to the elastic 
bloodvessels being thrown into vibrations by a forcible pulse wave. 

In Fig. 106 is shown the typical pulse wave of aortic regurgita- 
tion; and in Fig. 107 that of mitral stenosis, which is irregular in 
time and volume. (See page 273.) 

The force and rapidity of the pulse also depend largely on the 
condition of the bloodvessel walls, particularly the rapidity. The 






Fig. 106.— A tracing taken from a case of aortic regurgitation. Corrigau's pulse. Note the 
sharp upstroke and the sudden fall due to the blood falling back into the ventricle. 



Fig. 107. — The small pulse of mitral stenosis. 

latter also is influenced by the activity of the pneumogastric nerves 
in regulating the speed of the heart. Thus, if the arterial pressure 
be very high, through spasm of the arterioles, the difficulty experi- 
enced by the heart in forcing blood into the arteries will be so great 
that pulsation may be very slow, whereas if the normal resistance to 
the action of the heart be removed by vascular relaxation, the beat 
will be rapid, just as the wheels of a locomotive fly around on a 
slippery track when the friction or resistance is removed. If the 



276 



THE PULSE AND BLOODVESSELS 



vessels are relaxed, the impetus communicated to the column of 
blood in the vessels by the heart is lost, and so the pulse is not forcible; 
or if the resistance is excessive, the force is dissipated. 

The vagus or pneumogastric nerves are continually holding the 
heart in check, and by causing full diastole enable it to send out a 
large wave of blood at each contraction. If they are greatly stimu- 
lated, we have a very slow pulse and a full wave of blood with each 
heart beat ; but as the heart now beats very slowly the blood pressure 
may fall for lack of blood in the vessels, unless there is an increased 
force of the heart at each contraction to make up for the number of 
beats in the minute which have been lost, or unless there is also a 




Fig. 108. — Jacquet's sphygmocardiograph. 

great increase in arterial tension by contraction of the arterioles. 
A very slow pulse depends in the great majority of cases upon a high 
arterial tension from vascular spasm — i. e., resistance to the flow of 
blood ; more rarely it is due to irritability of the vagus nerves, pro- 
duced by pressure or disease, or by drugs, such as digitalis. 

The term "bradycaidia" is applied to a very slow pulse, which 
may be as slow as twelve beats a minute. 

A rapid pulse is seen most commonly as the result of stimulation 
of the heart by drugs, by fever, or by fear. Fear causes the vagus 
to lose control of the heart, and fever acts by reason of the stimulant 
effect of heat upon this viscus and its depressant effect upon the 



THE PULSE 277 

vagus. In other words, the quick pulse of fever is not a mere 
coincident symptom of fever, but the result of it. 

When the heart's action becomes exceedingly rapid it is called 
" tachycardia." It is due in the majority of instances to relaxation of 
the bloodvessels, and more rarely to depression of the pneumogastric 
nerves. As a symptom of organic disease it is a frequent manifesta- 
tion of exophthalmic goitre. Often in this condition the pulse 
becomes so fast that it cannot be counted. 

Great force of the pulse is due to hypertrophy, or overactioo of 
the heart because of stimulation; and great feebleness i> generally 
caused by marked dilatation not associated with hypertrophy, by 
chronic myocardial degeneration, and in acute disease by exhaustion 
of the heart muscle, or changes in the muscle fibers of the heart. 




Fig. 109. — Application of the sphvgmocardiograph of Jacquet to a case of aneurysm with 
systolic retraction at the apex. The recording apparatus is bound on the wrist as is the ordi- 
nary sphygmograph of Dudgeon. The radial pulse moves the lever nearest the arm, the jugular 
pulse is recorded by the lever attached by a tube to a tambour which is placed over the 
jugular vein and the apex beat by the lever nearest the wrist, which is connected by a tube 
to the tambour placed over the heart. 

There still remains for consideration those states in which circula- 
tory disturbances ensue as a result of incoordination between the 
auricles and the ventricles. Such a state may develop as the result 
of the action of large doses of digitalis and also in mitral stenosis in 
which disease it is very common. The most important state, how- 
ever, is that to which is given the name of the "Stokes-Adams syn- 
drome," in which there is not only incoordination between the auricle 
and ventricle, but the auricle may beat many times faster than the 
ventricle because of disease of the auriculo ventricular bundle of His. 
The general symptoms of this disease consist in a remarkably slow 
pulse, pulsation of the veins of the neck and sometimes attacks of 
vertigo, syncope and apoplectiform or epileptiform seizures. For the 
purpose of getting a graphic record of this state of the circulation the 
instrument called the sphygmocardiograph of Jacquet may be used 
(Figs. 108 and 109). By means of columns of air in tubes the impulse 



278 



THE PULSE AND BLOODVESSELS 



of the jugular vein and the apex beat are recorded by levers as in 
Dudgeon's sphygmograph and a third lever by pressure from the 



Shows the normal radial pulse on the lowest line, the apex beat on the middle line, the 
jugular pulse on the upper line. 



Fig. 110.— Tracings taken with tbe Jacquet apparatus. 

A tracing from a case of "Stokes-Adams disease," which shows below the very slow pulse 
and in the middle the slow apex beat and above the rapid and abnormal jugular pulsation due 
to the regurgitation from the auricle which is beating far oftener than the ventricle. 



radial artery produces a third tracing, each one being superimposed. 
(See chapter on the Thorax.) 



CHAPTER IX. 

THE A.BDOMEN AND THE ABDOMINAL VISCERA. 

The surface of the abdomen — Changes in the appearance and shape of the 
abdominal wall — The signs and symptoms of disease of the abdominal 
organs. 

The condition of the abdominal surface and abdominal contents 
is best studied by means of inspection, palpation, percussion, and 




CARTILAGE 
OF TENTH RIB 



HIGHEST LEVEL 
OF ILIAC CREST 



ANT. SUP. 
ILIAC SPINE 



Fig. 111. — -The regions of the abdomen and their contents. Edge of costal cartilages 
in curved outline. (Gray.) 

auscultation. For the purposes of inspection the surface of the 
abdomen has been arbitrarily divided by diagnosticians into a num- 
ber of spaces, which are best shown in the accompanying figure 
(Fig. Ill), and which get their names from the regions in which 



280 



THE ABDOMEN AND THE ABDOMINAL VISCERA 



they are located, or from the organ immediately underneath the 
abdominal wall. By means of these arbitrary outlines we can readily 
describe the exact spot in which a physical sign or symptom is found. 1 
The following table, from Gray's Anatomy, clearly shows the 
viscera to be found under each of the areas named : 



Eight Hypochondriac. 
The right lobe of the liver 
and the gall-bladder, hepatic 
flexure of the colon, and part 
of the ri^ht kidney. 



Right Lumbar. 
Ascending colon, part of the 
right kidney, and some con- 
volutions of the small intes- 
tine. 



Sight Inguinal (Iliac). 
The caecum, appendix cseci. 



Left Hypochondriac. 
The splenic end of the stom- 
ach, the spleen and extremity 
01 the pancreas, the splenic 
flexure of the colon, and part 
of the left kidney. 

Left Lumbar. 
Descending colon, part of the 
omentum, part of the left kid- 
ney, and some convolutions of 
the small intestine. 



Left Inguinal (Iliac). 
Sigmoid flexure of the colon. 



Epigastric Region. 
The pyloric end of the 
stomach, left lobe of the liver, 
and lobulus Spigelii. the pan- 
creas, the duodenum, parts of 
the kidneys and the supra- 
renal capsules. 

Umbilical Region. 
The transverse colon, part of 
the great omentum and mes- 
entery, transverse part of the 
duodenum, and some convo- 
lutions of the jejunum and 
ileum, part of both kidneys. 

Hypogastric Region. 
Convolutions of the small 
intestine, the bladder in chil- 
dren, and in adults if dis- 
tended, and the uterus during 
pregnancy. 

Inspection. — On inspecting the abdominal surface the physician 
should look for eruptions which may indicate some general disease, 
as typhoid fever; for localized swelling, which may be due to hernia; 
for striae, indicating that the skin has been stretched by excessive 
fat, by great swelling from ascites, or by pregnancy. He should also 
in a case of suspected early pregnancy look for the dark streak in the 
median line. If the umbilicus is protruding and tense it may indicate 
distention due to grave abdominal disease, or it may be infiltrated by 
a morbid growth which has been primarily hepatic. If it be a sec- 
ondary growth the navel will perhaps be " moored fast." Sometimes 
it is much swollen from chafing and eczema. Umbilical hernia may 
be found. 

The general abdominal wall is protruded and retracted in normal 
respiration in both sexes, but more markedly so in males. It is 
pushed outward, or protruded, by many perfectly normal causes, 
such as an unusual amount of fat in the omentum, pregnancy, and 
an accumulation of liquid and food in the stomach after a heavy 
meal. It is also convex to an abnormal degree in cases in which 
ascites is present, when the stomach and bowels are overdistended 
with gas (tympanites), and when any of the organs found in the 
peritoneal cavity are the seat of swellings or tumors of large size. 
In children a protruding pot-belly, "the frog-belly" of the French, 

i For changes in the skiu of the abdomen, see chapter on the Skin. 



TYMPANITES AND ASCITES 281 

is seen in cases of scrofula or tuberculosis of the mesenteric glands, 
and in those cases which suffer from chronic gastro-intestinal 
catarrh. It is claimed in a recently published paper by a French 
clinician that the intestinal canal is not only dilated, but of greater 
Length than is normal in these cases. 

If the belly wall is retracted, concave, or "scaphoid," as it is some- 
times called, we look for the cause in abstinence from food, or 
remember the possibility that excessive vomiting or purging may 
have emptied the gastro-intestinal tract of its usual contents. We 
also find a retracted belly wall in nearly all cases of advanced 
wasting diseases, such as carcinoma, peritoneal tuberculosis of the 
cirrhotic type, or tuberculosis of the lungs; and if the retraction is 
associated with muscular rigidity of the belly wall and pain, we sus- 
pect the early stages of peritonitis or the presence of some acutely 
painful affection, such as renal or hepatic colic or lead colic. Marked 
concavity and retraction of the belly wall arc also -ecu sometimes in 
cases of tuberculous meningitis. 

Sometimes in thin patients with some atrophy of the abdominal 
muscles peristaltic waves are to be seen traversing the abdominal 
surface as the result of violent movements of the bowels. These 
waves are commonly seen in cases of intestinal obstruction, and in 
neurotic persons with mucomembranous enteritis, or, if in the 
epigastrium, may be due to a dilated stomach. If the waves are 
from below upward and in the right side, they are probably arising 
in the ascending colon; if from above downward and in the left 
side, in the descending colon and sigmoid flexure. Again, gastric 
waves pass from left to right, while those in the transverse colon 
pass from right to left. 

Tympanites and Ascites. — The abdomen is distended very greatly 
by gas in many cases of peritonitis, typhoid fever, and in persons 
suffering from flatulent colic. If this be the cause of the distention. 
percussion of the anterior and lateral belly wall when the patient 
is lying on the back will give a tympanitic note. We separate, diag- 
nostically, the swollen abdomen due to wind from that due to ascites 
by the fact that in the latter condition the epigastrium is moderately 
flat when the patient is lying down, while when tympanites is present 
it is more protruding. Again, in ascites the greatest bulging is gen- 
erally to be found in the flanks, or, if the patient sits or stands erect, 
the hypogastric region bulges from the change in the position of the 
fluid. If the swelling be due to a moderate-sized ovarian cyst, this 
variation in form will not occur, as the cyst is not readily movable. 
If the ovarian tumor be large, the differential diagnosis may be 
most difficult and almost impossible, except by the history or by 
examining the liquid withdrawn by tapping. 

In cases of ascites due to free liquid in the abdominal cavity per- 



282 THE ABDOMEN AND THE ABDOMINAL VISCERA 




Fig. 112. — Enormous ascites. The area inside the line is that which was resonant on per. 
cussion (gut tympany)- On either side and below the line there was absolute flatness due to 
the presence of fluid. (From the author's wards.) 




Fig. 113. — Same as Fig. 112. When the patient was turned on the side the fluid flowed 
in that direction, and so the area of resonance was altered, the area of flatness on the right 
increasing and on the left diminishing. 



TYMPANITES AND ASCITES 



283 



(Mission will elicit flatness over the flanks and resonance where the 
intestines containing gas are floated up against the anterior belly 
wall above the effusion. Sometimes, however, if the large intestine 
be empty of fecal matter, percussion in the flank behind the mid- 
axillary line will reveal tympany, because the peritoneum walls off the 
liquid from the posterior surface of the bowel. If the patient is 
turned slightly to one side, the area of flatness on percussion is 
altered, as is shown in Fig. 113. Palpation will also reveal fluctua- 
tion in ascites, but none in tympanitic distention. To develop this 




Fig. 114. — Showing method of determining the presence of fluid in abdomen by transmitted 
fluctuation. The hand of an assistant is placed on edge on the middle line, to prevent trans- 
mission of impulse by the belly wall. The right hand then taps the flank, and if fluid is 
present the impulse is felt by the left hand on the other side. 



fluctuation, the patient is placed on his back and the finger tips of the 
left hand of the physician are placed against the skin of the flank. 
With the finger tips of the right hand the opposite flank of the patient 
is struck a blow as in performing ordinary percussion, when the 
impulse, if fluid is present, will be transmitted to the fingers of the 
left hand. To prevent a transmission of the impulse through the 
abdominal wall, an assistant may press with the edge of his hand 
over the linea alba (Fig. 114). As the result of gradually increasing 
intra-abdominal pressure the floating ribs become pushed outward, 



284 THE ABDOMEN AND THE ABDOMINAL VISCERA 

the apex beat of the heart is often displaced upward and outward, 
and the umbilicus becomes protruded instead of retracted. The 
skin of the belly wall becomes thin and shining, and the recti muscles 
may become separated. After tapping in such cases the peristaltic 
movements of the bowels can be readily felt through the intervening 
skin. 

Having decided that the distention is due to an accumulation of 
free fluid in the abdomen, it remains for the physician to determine 
what the cause of the ascites may be. Its most frequent cause is 
atrophic cirrhosis of the liver, which results in engorgement of the 
abdominal vessels with secondary transudation of fluid. (See Fig. 114.) 
If it be not due to cirrhosis, it may arise from an abdominal tumor, 
which by pressing on large vessels results in an effusion of liquid 
through their walls (see Plate IX), or be caused by tuberculous peri- 
tonitis, by obstruction of the thoracic duct, by valvular disease of 
the heart causing an obstruction to the flow of blood in the vena cava, 
or, finally, by chronic parenchymatous nephritis. If the last cause 
be present, there will be some edema of the lower extremities or 
general anemia with dyspnea and albuminuria. For the typical 
symptoms and physical signs of these various affections the reader 
is referred to those parts of this book in which they are discussed. 
(See Index.) 

There is an additional source of information to be utilized as to 
the cause of the ascites, namely, the character of the effusion. If 
the fluid withdrawn on aspiration has a specific gravity of 1.008 and 
contains but a trace of albumin (about 0.97 per cent.), it is probably 
due to hepatic cirrhosis; whereas if due to the pressure of a tumor 
the specific gravity is usually about 1.012 and the albumin nearly 2 
per cent. Such a specific gravity and proportion of albumin may 
also result when the ascites is due to heart disease or to pressure on 
the thoracic duct. When the effusion is the result of Bright's disease 
the specific gravity is apt to be only 1.006 and the proportion of albu- 
min only a trace. In cases in which the ascites arises from some 
disease directly affecting the cells lining the peritoneal cavity, as 
carcinoma of the peritoneum or of the abdominal viscera, or tuber- 
culous peritonitis with or without pus, the specific gravity is much 
higher than just stated, namely, from 1.018 to 1.027, as a rule, and 
the proportion of albumin ranges from 3.80 in the case of growths to 
5.76 in the case of tubercle and 7.10 when there is pus. To express 
it otherwise, the percentage of albumin is in direct proportion to the 
inflammatory process, and an effusion due to hydremia would there- 
fore contain only a trace of albumin. Further than this, it is asserted 
by Pohl and Rosenbach that the effusions due to venous engorge- 
ment, heart disease, and renal lesions can be separated from those 
due to disease in the peritoneum affecting this membrane directly 



PLATE IX 




Median Vertical Sec-tion of Body of a Boy of Seventeen, who Died of Colloid 
Cancer of the Peritoneum and Iliac Flexure. 

The gelatinous masses represent the growth and the ascitic fluid is readily seen. (Ponfick's Atlas.) 



TYMPANITES AND ASCITES 285 

by a test following the administration of iodide of potassium. When 
this drug is given to the first class of cases it speedily appears in the 
effused fluid; but should effusion be due to the organic diseases of 
the peritoneum which have been named, it will not appear. The 
fluid to be tested is placed in a test tube and some nitric acid and 
chloroform added, when if iodine is present its characteristic color 
will appear. Should the cause of the ascites be a ruptured ovarian 
cyst the diagnosis of its cause, except from the history of a previous 
localized swelling, is exceedingly difficult. The fluid under these 
circumstances is usually of a specific gravity of L.026, but its specific 
gravity may be much lower. It is asserted that in the instances in 
which the specific gravity of the fluid is very low the swelling is due 
to a cyst of the broad ligament. 

Rotmann asserts that in all serous effusions, even in non-diabetic 
patients, there is present a trace of sugar; whereas in all seropurulent 
effusions sugar is absent. 

Very often in cases of ascites, particularly when this condition 
arises from hepatic cirrhosis, there is developed on the anterior 
belly wall a more or less well-defined bunch of vein-, which is some 
times called the caput Medusa*, as the result of an attempt at collateral 
circulation, to compensate for the obstructed flow caused by the 
changes in the liver. Sometimes a mediastinal growth will cause a 
somewhat similar development. When the obstruction is lower 
than the liver the superficial veins of the lower part of the abdomen 
(hypogastrium) will be found distended. 

Localized bulging of the abdominal walls, chiefly on the right 
side, is found in cases in which the liver is enlarged by hypertrophic 
cirrhosis, or bv cancer or other morbid growth, such as gumma or 
sarcoma, and by abscess. The swelling, if its origin be in the liver, 
will arise under the floating ribs on the right side, and will extend 
downward and forward toward the umbilical area. If the enlarge- 
ment be great, it will extend far below the umbilicus and across 
the umbilical area to the opposite side of the abdomen. In 
enlargement of the spleen similar signs, springing from the floating 
ribs w T ell over to the left side, may be developed usee Fig. 115), and 
large cystic kidney on either side may cause abdominal bulging, 
particularly if the kidneys be floating. (See Floating Kidney and 
Spleen.) 

Marked swelling of the epigastrium indicates distention of the 
stomach bv gas or food, or that this organ is the seat of morbid 
growth. Sometimes a similar distention results from enlargement 
of the posterior mediastinal and retroperitoneal glands. Again, 
distention of the epigastrium is apt to be caused by enlargement of 
the left lobe of the liver. In ovarian tumors the growth often gradu- 
ally distends the entire belly equally; but, as already stated, the 



280 THE ABDOMEN AND THE ABDOMINAL VISCERA 

history is usually that of swelling, low down, and of its being chiefly 
unilateral at first. 

It should be remembered that the discovery of a pyriform 
swelling in the hypogastrium may possibly be due to a pregnant 
uterus, or to retention of urine, with consequent distention of the 
bladder. 

Cases of dilatation of the stomach often show very great bulging 
of the umbilical area of the abdominal wall when that viscus is dis- 
tended by liquid and gas. (See Percussion in this chapter.) 




Fig. 115. — A case of splenic anemia with great enlargement of the spleen, as shown in the 
large outlined area. The smaller outlines indicate the areas of anemic murmurs near the 
base of the heart and in the carotid artery. (From the author's wards in the Jefferson Medi. 
cal College Hospital.) 

In inspecting abdominal swellings the physician should watch to 
see if they move up and down with respiration. If they do, they 
are probably connected with the diaphragm and depend upon disease 
of the liver and spleen, as tumors of the pancreas, stomach, and 
kidney are usually not attached to the diaphragm, and therefore 
generally do not move. Inspection of the abdominal wall will also 
show possible venereal infection if the glands in the groin are en- 
larged, or if in suppurating they have left puckered scars. If silvery 
lines extend across the belly, they may indicate pregnancy past or 
present, or any state of the abdominal tissues causing great stretching 
of the skin. Great bulging in the neighborhood of the umbilicus 



PALPATION AND PERCUSSION 287 

will naturally suggest umbilical hernia, and -welling in the groin, 
adenitis, inguinal hernia, or perhaps an appendicular abscess. 

Palpation and Percussion. — More important than any other exter- 
nal method of studying the condition of the abdominal content- is 
the use of gentle palpation, the fingers being gradually worked down 
into the abdominal cavity in such a way as not to cause pain or 
excite the muscles of the abdominal wall to resistance. The hand 
should always be carefully warmed before palpation is attempted, 
and the object of the examiner is to discover, first, the hardness or 
resistance to pressure; secondly, the consistency and form of the 
organs which he can touch; and, thirdly, whether any swellings 
which he feels are movable, bound down and immovable, pulsating, 
soft or hard, nodular or smooth. The patient whose abdomen i- to 
be palpated must be placed flat on his back, with the knees drawn up 
to relax the abdominal muscles, the head and neck should be raised, 
and, if possible, the attention of the patient should be diverted by 
conversation about some symptom which exists elsewhere than in 
the belly, while the examination is made, as in this way voluntary 
muscular resistance is removed to some extent. He should be made 
to breathe easily through his opened mouth; and if the belly wall 
remains so rigid that a perfect examination is impossible, and yet the 
results of such an examination are very important, ether or chloro- 
form should be given to relax the muscles. In other instance- in 
which it seems inadvisable to give an anesthetic, the patient may be 
placed in a bath as hot as he can bear. He should be entirely sub- 
merged up to the neck. The hot bath often relaxes the abdominal 
wall sufficient to aid diagnosis very greatly. 

After the abdominal contents have been carefully examined, the 
patient being on his back, he should be placed first upon his left side 
and then upon his right, and the abdominal contents again palpated. 
This is particularly necessary when examining the belly for growths 
or when enlargement or displacement of the liver, spleen, or kidneys 
is suspected. 

It must be remembered, however, that the anterior abdominal 
wall, particularly that of nervous persons, is often very sensitive or 
"ticklish," and the mere exposure of the skin to the air of the room, 
coupled with the fear of examination, may cause great rigidity of the 
belly wall without there being any abnormal condition present. 
This can be generally overcome by gentleness in palpation and 
by resting the palm of the hand on the belly and partly flexing the 
fingers, rather than by attempting to insert the finger tips between 
the abdominal muscles. The writer has seen a case of rhythmical 
hysterical spasm of the recti muscles in a male, which at first gave 
the sensation of an enormous diffuse pulsating aneurysm of the 
abdominal aorta. 



288 



THE ABDOMEN AND THE ABDOMINAL VISCERA 



Peritonitis. — Great resistance of the rigid abdominal muscles is 
found whenever peritonitis is present in an acute form, in some cases 
of renal and hepatic colic, and more commonly in lead colic and in 
hysteria. In peritonitis great tenderness to the slightest touch is also 
present. Another symptom of acute peritonitis, aside from the ex- 
quisite tenderness of the abdomen, the drawn lip, the thirst, and the 
distention or rigidity of the belly wall, is pain of a severe character; 
unless it be septic peritonitis, when pain may be absent. There are 




Fig. 116. — McBurney's point of great tenderness in appendicitis. 

also the drawing up of the limbs to relieve abdominal tension, obsti- 
nate constipation, moderate fever, and a very rapid, quick pulse. 
The tongue speedily becomes dry and parched, and collapse may 
soon ensue in severe cases. It is not to be forgotten that localized 
peritonitis may result from many causes, usually from disease of the 
appendix vermiformis or the geni to-urinary tract in women, and 
that the local symptoms and lesions may be limited by a wall of 
lymph to a very small area of the abdominal cavity. 



ABDOMINAL TUMOR 289 

Appendicitis. — Jn appendicitis rigidity may be general if the 
inflammation is widespread, or localized if the original area is limited 
or walled off from the rest of the abdominal cavity. If the rigidity 
be due to peritonitis, secondary to appendicitis, the following symp- 
toms will point to an inflammation of the appendix as the cause: 

There is usually a rapid pulse, which becomes more and more 
speedy as the gravity of the case progresses. Indeed, a very rapid 
pulse is a sign of great importance as indicative of the seventy of the 
malady. There is marked tenderness at McBurney's point (Fig. 
11(3) on pressure with the finger tip. The pain may be referred to 
the epigastrium and the sigmoid flexure as well, but is not so severe 
on deep pressure in these parts. There is usually an increased leuko- 
cytosis (see chapter on the Blood), an anxious face, and sometime- 
very great pain. (See chapter on Pain.) The febrile movement is 
usually moderate, and it may be absent. It is to be constantly borne 
in mind that the early stages of typhoid fever often so closely simulate 
appendicitis of the subacute type, that a differential diagnosis can 
only be reached after a most careful study of the case. 

Abdominal Tumor. — Let us suppose that on placing the hand upon 
the epigastrium and the upper part of the umbilical area we find a 
swelling. In the first place, we must decide as to whether it is in the 
abdominal wall or in the abdominal cavity. If it is in the wall, it 
will be movable with the tissues of the wall and readily grasped by 
deep palpation; but if in the abdominal cavity the abdominal wall 
may be made to move over it unless it be attached to the parietal 
peritoneum. 

Let us suppose it is in the wall of the abdomen, What can the swell- 
ing be? It may be a fatty tumor; in which case its surface will be 
dimpled and resistant, probably not painful, unless the part has been 
inflamed by rubbing or an injury, and it will not fluctuate. There 
will generally be a history that the person has exercised constant 
pressure on the part, as in Leaning against a bench or table. Again, 
it may be an abscess; but aside from the rarity of this condition, we 
can exclude such a possibility by the absence of pain and fluctuation, 
and the absence of a history of a severe injury. 

Very much more commonly a swelling in the epigastrium, or 
upper umbilical area, is due to an intra-abdominal cause. In adults 
the most common cause is probably a growth (generally a carcinoma) 
of the pyloric end of the stomach or an indurated gastric ulcer may 
be present. In other instances it is due, particularly in children, 
to enlarged lymphatic glands, as in tuberculous disease of the mesen- 
tery. This is also sometimes seen in adults. Sometimes by reason 
of tuberculous peritonitis a nodular mass is not only felt in this area, 
but an abscess containing tuberculous pus may be formed and 
become surrounded by walls formed by the gluing together of the 
19 



290 Til E ABDOMEN AND THE ABDOMINAL VISCERA 

organs by lymph. Carcinoma of the pancreas may also cause a 
swelling in this neighborhood, or a cyst of the pancreas may be 
present. Aneurysm of the abdominal aorta is also not to be for- 
gotten. Sometimes, too, a distended or carcinomatous gall-bladder 
mav project into this area. (See below.) 

Gastric Carcinoma. — If the growth be gastric carcinoma, the patient 
will be in or past middle life (probably between the fortieth and 
seventieth years, although cases may occur as early as thirty years) ; 
will have a history of constantly increasing discomfort in the stomach; 
there will have been much sour belching, and perhaps vomiting of 
coffee-ground-looking material; marked loss of flesh and some 
cachexia will be present. The disease occurs twice as frequently in 
men as in women. According to Welch's statistics, out of 1300 cases 
of gastric cancer, 791 were in the pylorus, 148 in the lesser curvature, 
104 in the cardia, 68 in the posterior wall, and 61 involved the whole 
stomach. The remainder were in the fundus, the greater curvature, 
or the anterior wall. The growth, if in the pylorus, is usually freely 
movable, and for this reason can be readily felt, and then is often 
momentarily lost to palpation. Its position is apt to change with the 
posture of the patient and the presence or absence of food in the 
stomach. Pain is usually elicited on deep pressure, and, if the growth 
be large and at the pylorus, the symptoms of dilatation of the stomach 
may be present, because that viscus is dilated through obstruction 
of the pyloric opening, which results in retention of the gastric 
contents. 

Similar symptoms may, however, be produced by a deposit of 
inflammatory lymph around a pyloric ulcer, which being changed 
into fibrous tissue, causes great thickening of the gastric wall with 
matting of the omentum around it, closely simulating the mass pro- 
duced by a malignant growth or simple hypertrophic pyloric stenosis. 
When cancer involves the cardiac area of the stomach, this organ, 
instead of becoming dilated, becomes greatly diminished in size, and 
feels like a narrow band in the neighborhood of the left floating ribs 
and epigastrium. The diagnosis will be aided by discovering that 
the capacity of the stomach is very small and hydrochloric acid 
absent. 

But the presence of a tumor which can be palpated in the neigh- 
borhood usually occupied by the stomach does not, of necessity, indi- 
cate that this viscus is diseased. Not very infrequently an abnormal 
position of the colon or of other portions of the viscera may result 
in the physician's mistaking a growth in these parts for a gastric 
cancer. Even carcinomatous lymph glands may lead to this error. 
It is in these cases that the testing of the stomach contents is most 
useful in making a differential diagnosis. Thus, if the normal gastric 
acidity be present we can exclude gastric carcinoma; even if the 



GASTRIC ULCER 291 

growth be carcinoma of the duodenum, the gastric juice usually 
remains normal. Not only does the examination of the gastric 
contents aid us hi this manner, but if a growth in the duodenum 
causes stricture, it may cause the duodenal contents to regurgitate 
into the stomach, so that we find pancreatic digestion going on there. 
Boas asserts that the presence of some liquid brown fecal fluid in the 
Stomach indicates jejunal stricture. 

In considering the differential diagnosis of carcinoma of the stom- 
ach and bowel, it is to he remembered that the former is far more 
common than the latter. Thus Heimann found that out of 20,054 
cases dying of carcinoma in the hospitals of Prussia, 10,537 involved 
the digestive tract, and of these, 4288 affected the stomach, whereas 
only 20 involved the small intestine and 224 the large intestine. 

Gastric Ulcer. — Sometimes in cases of chronic gastric ulcer the area 
involved becomes so indurated as to be felt as a hard mass through the 
abdominal wall. In such instances the points which aid us in sepa- 
rating the condition from gastric cancer are the fact that the patient 
is young and usually a woman ; that the vomiting occurs immediately 
after taking food, for in gastric cancer it is only seen in most cases 
several hours after food has been taken; that there is no sign of 
gastric obstruction; that there is an excess of hydrochloric acid in 
the gastric contents in cases of ulcer, and an absence of this acid in 
cases of cancer. It is, however, a noteworthy fact that if the cancer 
involves only the pylorus, the acid may be present, because this 
part of the stomach is not that which secretes acid; and it is also 
to be remembered that a single test of the gastric contents is not to 
be depended upon, but that several should be made. (See tests 
for HC1 in this chapter.) Any disease which produces atrophy 
of the gastric tubules may cause an absence of hydrochloric 
acid, as, for example, grave pulmonary tuberculosis and renal 
or cardiac disease. Even catarrhal jaundice may temporarily 
arrest its secretion, and as jaundice is often present in gastric 
carcinoma, because of pressure or hepatic involvement, this fact 
should not be forgotten. In other words, the absence of hydro- 
chloric acid is not pathognomonic of cancer; neither is its presence a 
guarantee of the absence of the growth. The result of an examina- 
tion for this acid simply gives us additional evidence in making a 
diagnosis. As a rule there is no cachexia in cases of gastric ulcer, 
though there may be marked anemia. There is usually in cases of 
ulcer no great loss of weight unless the symptoms have been present 
a long time. In gastric ulcer vomiting of blood may occur, whereas 
in gastric cancer if blood is present it is broken-down blood and 
resembles coffee grounds. (For the examination for occult hemor- 
rhage, see chapter on the Bowels and Feces.) 

In cases of gastric ulcer great pain is often produced by deep or 



292 THE ABDOMEN AND THE ABDOMINAL VISCERA 

even superficial pressure over the epigastrium, and a painful spot can 
generally be found on the back, about the angle of the right scapula. 

These painful spots are, however, as a rule quite localized, and the 
fact that they are very painful at one particular spot, and yet the 
surrounding parts are comparatively insensitive, points to ulcer as a 
cause. 

It is worth remembering, however, that duodenal ulcer may 
cause identical symptoms on palpation. Diffuse tenderness in this 
area is more apt to be due to colitis or even to appendicitis or 
sigmoiditis, which often results in pain in this area or in tenderness 
on percussion. 

Disease of the Gall-bladder. — A very more frequent lesion in the 
epigastric area, or so near to it as to lead the physician to consider 
it epigastric, is disease of the gall-bladder. Theoretically the area 
of the gall-bladder is distinctly to the right of the median line, but 
in women whose lower ribs have been compressed by corsets the 
gall-bladder is pushed inward, and, it may be, distinctly downward. 
Because of these facts, and because carcinomatous disease of the 
stomach and gall-bladder have a direct etiological relationship, the 
possibility of an epigastric mass being a gall-bladder growth must 
always be considered. As a rule, however, disease of the gall- 
bladder is discovered while palpating the lower border of the liver. 
If the mass is of good size and the abdominal wall thin, it will be 
felt as a pyriform body and may be slightly fluctuating. Such a 
mass is probably a distended gall-bladder, and it may be associated 
with enlargement of the liver and jaundice. The causes of enlarge- 
ment of the gall-bladder are several, viz., distention from the accu- 
mulation of bile produced by obstruction in the cystic or common 
duct, or the presence of a large number of calculi in the gall-bladder, 
and often to the accumulation of thin mucus, which may or may not 
be bile-stained, the so-called "hydrops of the gall-bladder." The 
causes of acute obstruction of the ducts are gallstones, new-growths, 
such as carcinoma and rarely gumma, and inflammatory processes 
in the ducts themselves, with inflammation in surrounding tissues 
and organs. Often the inflammatory processes just named will have 
been produced by the presence of gallstones, which may, by causing 
ulceration of the mucous membrane, permit severe infections to 
take place. Rarely is it due to ascarides or echinococcus. (Cour- 
voisier states the proportion to be in 74 cases, 57 due to stone, 7 to 
ascarides, and 3 to echinococcus.) The question then arises as 
to the cause of the enlargement in the particular case at hand. 
Obstruction of the bile ducts is, as already stated, due, in the vast 
majority of cases, to stone, aside, of course, from that due to an 
acute catarrh which is but temporary in its effects, and therefore 
the probable cause in every case is stone. If this is the cause, the 



DISEASE OF THE CALL HI. ADDER 293 

patient may give the history that at some time in the near or remote 
past, after a period of more or less distress in the hypochondrium, 
she has been seized by a pain which was paroxysmal in type and 
extended backward and upward to the region of the scapula or 
shoulder. This pain was also peculiar in that it was apt to occur 
at night rather than after taking food, as in gastric cancer or ulcer, 
because the bile is flowing to the gall-bladder at this time, instead 
of directly into the bowel. Examination at such times may have 
revealed a swelling of the gall-bladder. There may be, but often 
there is not, a history of jaundice. Manifestly this is a history of an 
attack or attacks of gallstone colic, and should lead us to the belief 
that the enlargement of the gall-bladder is due to stone, but it may 
be due to a malignant growth. In this connection it is well to take 
into consideration the importance of the presence or absence of jaun- 
dice at this time, and this is well expressed by Mayo Etobson in 
the words: "Jaundice with distended gall-bladder is presumptive 
evidence of malignant disease, but jaundice without distended gall- 
bladder favors the diagnosis of cholelithiasis." This i> sometimes 
called " Courvoisier's law r ." In other instances there may be no 
history of attacks of gallstone colic, the patient simply complaining 
of pain and discomfort in the hepatic area. Not rarely these 
attacks of pain are regarded by patient and physician as being due 
to indigestion, gastric or intestinal. 

It is important to remember that in some cases of enlargement of 
the gall-bladder due to obstruction of its duct the enlargement 
may be so gradual and so great that the distended viscus may be 
felt far from its normal site in the middle line or even under the 
left ribs. 

An additional symptom favoring gallstone as a cause is fever, which 
is due to infection produced by the stone injuring the mucous 
membrane. Sometimes it is simply an indication of inflammation, 
at others it indicates anything from mild purulent infection of the bile 
passages to empyema of the gall-bladder or a general cholangitis. 
If the infection be with a benign organism, the symptoms may be 
mild; but if it be due to the more malignant forms it is often viru- 
lent, and the febrile movement most severe. Much depends, too, 
upon the freedom of drainage. It the gall ducts permit the escape 
of the pus into the gut, the symptoms may become greatly reduced; 
but if it be retained they are apt to become more pressing. (See 
Cholangitis, in chapter on Fever.) 

When the gall-bladder is distended with gallstones there is often 
a history of colic; there may be gallstone crepitus on careful palpa- 
tion, and symptoms of fever due to a cholecystitis set up by the 
stones. It is not to be forgotten that gallstones are present in about 
10 per cent, of all adults, although, as Kehr has well pointed out 



294 THE ABDOMEN AND THE ABDOMINAL VISCERA 

fully 95 per cent, of such persons come to autopsy from other causes 
without even suffering from any manifestation of their presence. It 
is only when the calculus produces irritation or mechanically blocks 
the ducts that symptoms develop. 

A new-growth by pressing on the gall ducts may obstruct the flow 
of bile and produce jaundice, and a mass; but there is usually no 
paroxysmal pain, and the growth is usually secondary to a growth 
elsewhere in neighboring parts, which may be demonstrable, Rare 
as is primary malignant new-growth of the gall-bladder, it is almost 
unknown in the liver, but it may be secondary to a gastric carcinoma 
which is small in size whereas that in the liver may be a large growth. 

The general cachexia, rapid loss of weight, and the age of the 
patient may aid the diagnosis of the tumor, and in this respect Cour- 
voisier's law is to be recalled. 

Pancreatic Carcinoma. — The presence of a resisting mass, deeply 
situated in the epigastrium, or the upper part of the umbilical area, 
and felt only on deep palpation, and then often indistinctly, should 
bring before the mind the possibility of the presence of carcinoma of 
the pancreas, a diagnosis which will be largely confirmed if cachexia 
be asserting itself, if there be great pain in this neighborhood, and 
if there are oily stools after fats are taken, as a result of the absence 
of pancreatic juice. Still further confirmation of this diagnosis will 
be present if diabetes mellitus develops (pancreatic diabetes). Such 
a growth in the pancreas is usually a scirrhous cancer, and may be 
primary or secondary. Segre found that of 627 cases of carcinoma 
of the upper abdominal organs, cancer of the pancreas occurred in 
127, but in only 12 of these primarily. Stiller asserts that the fol- 
lowing symptoms are fairly sure signs of pancreatic cancer, namely, 
marked dyspepsia, rapid emaciation and cachexia, subnormal 
temperature, persistent and progressive jaundice without hepatic 
enlargement, but often with swelling of the gall-bladder from obstruc- 
tion to its duct. These signs are, of course, only of value if the 
evidence of malignant growth elsewhere can be excluded. 

Not rarely a mass, or masses, are felt in the abdomen which may 
be due to tuberculosis of the omentum, which causes a drawing up 
or puckering of the membrane, so that there can be felt a firm 
mass extending across the upper abdominal zone. Sometimes it can 
be felt to the right or left of the middle line. In other cases, but 
rarely, we find retracted and thickened coils of intestine which feel 
like tumor masses, and these are apt to be drawn against the spine, 
so that the belly is very scaphoid and empty. We also meet with 
cases in which large tuberculous growths of the mesenteric glands 
occur. In the last group of cases and in those of the omental type, 
named above, there may be some ascites. 

Finally before dismissing the important subject of swelling and 



GASTRIC DILATAT10X 295 

tumor in the upper abdominal zone it is necessary to recall the fact 
because of the close juxtaposition of many organs in this area an 
exact diagnosis may he impossible, so far as a diagnosis of the 
actual lesion is concerned and yet a sufficiently accurate diagnosis 
may be made to direct treatment. Thus a chronic inflammatory 
process above the gall-bladder may by involving the pylorus in 
its adhesions and exudations cause signs of gastric dilatation and 
obstruction, or again a history which seems characteristic of gall- 
stone colic is really due to ulcer of the pylorus. Further than this 
it is to be recalled that all these facts are in health quite movable 
and in disease are often found far from their normal sites. Thus 
the pylorus may be anchored high up in the belly by adhesions or 
dragged into the umbilical area by the weight of a growth. 

Gastric Dilatation. — Gastric dilatation results from obstruction of 
the pylorus or from inherent feebleness of the stomach wall, and 
when it is present the entire upper part of the abdomen may be 
found distended, and tense but yielding. The history will show that 
the patient is attacked now and again by vomiting, during which 
a most extraordinary quantity of food and liquid, which has gradu- 
ally accumulated, will be expelled. 

We discover the condition of the stomach as to its size and shape 
by means of washing it clean with the stomach tube and then filling 
it with a known quantity of water, which can be siphoned out and 
measured. Or instead we first wash out the stomach by means of a 
stomach tube and then fill it with gas by giving the patient to drink, 
first, a half-glass of water with 1 dr. of sodium bicarbonate in 
it, and then another half-glass with 30 gr. of tartaric acid dis- 
solved in it, so that gas will distend the viscus. ( me is able with ease 
in a thin person, by means of percussion, to outline the stomach by 
the area in which a high-pitched tympanitic note is heard. It is 
best to mark the edge of gastric resonance by means of a blue pencil, 
and thus map out the gastric area. Instead of this, we may 
distend the stomach with air by attaching a Davidson syringe 
to a stomach tube or by using an atomizer bulb for the pumping 
purposes. 

Even before the stomach is artificallv distended with gas percus- 
sion may give us valuable information, for if obstruction of the 
pylorus exists, there may be found either a large area of gastric 
tympany through the accumulation of gas from fermentation, or, if 
no vomiting has taken place for some time, an equally great area of 
gastric dulness due to an accumulation of food and liquid. If there 
is a growth at the pylorus causing obstruction, there will be impair- 
ment of resonance wherever the pylorus may be situated. While 
this is a somewdiat indefinite statement, it is to be remembered that 
a more definite one is liable to mislead the student, for even in health 



296 



THE ABDOMEN AND THE ABDOMINAL VISCERA 



the position of the pylorus changes greatly when the stomach is 
empty or is filled with food. Thus, when empty the viscus hangs 
with the pylorus very low, but when it is filled the pylorus is raised. 
Fig. 117 shows the normal gastric area when the stomach is dis- 
tended with gas. 

In other instances we can use the so-called gastrodiaphane of 
Einhorn, which consists of a small electric lamp, protected by strong 
glass, and attached to a rubber tube which contains the necessary 




Fig. 117. — Outline of normal position and size of an adult stomach when distended with gas. 

wiring for the electric current, and which is swallowed just as is the 
ordinary stomach-tube. The stomach should first be thoroughly 
cleansed by lavage, then filled with pure water and the lamp swal- 
lowed. If the patient be moderately thin and the inspection is made 
in a dark room, the outline of the lighted stomach can be seen through 
the abdominal wall and some idea of its dimensions obtained. Nor- 
mally, the greater part of the stomach will be found to the left of the 



GA STRIO ML A TA TION 



297 



middle line and about one to two inches above the umbilicus. (See 
Percussion.) 

An improved and more thorough method of carrying out this plan 
of examination is by the use of fluoresein. The patient is given 
2 gr. of quinine bisulphate three times a day for twenty-four hours 
before the examination is made. He then swallows a tumblerful of a 
solution of sodium bicarbonate in distilled water (35 gr. to the pint) 




Fig. 118. — Showing the change in the position of the stomach in dilatation, and how 
difficult it is for this organ to empty itself of fluids. 

and follows this by another tumblerful of another solution made 
by adding 2 fl. dr. of glycerin, \ gr. of fluoresein and 35 gr. of 
sodium bicarbonate to a pint of distilled water. If after this is done 
the gastrodiaphane is introduced it is said to greatly increase the 
degree of illumination. In a limited use of the gastrodiaphane, with 
and without fluoresein, I have not been impressed w T ith its value, but 
a larger experience may give better results. 



298 THE ABDOMEN AND THE ABDOMINAL VISCERA 

Another very valuable method of determining the presence of 
gastric dilatation and gastroptosis is by the employment of the x-ray 
and large doses of bismuth, which substance is used because it renders 
the gastric walls opaque. ^ The dose of bismuth must be massive, 
as much as 2 oz. mixed with mashed potato or held in suspension in 
a pint of mucilage of acacia. After the examination the bismuth 
must be withdrawn by a stomach tube to prevent bismuth poison- 
ing. The best results are naturally obtained when the patient is in 
the erect position. Either the fmoroscope or the radiographic plate 
may be employed. Usually it is best to use both methods. 




Fig. 119. — Gastroptosis and enteroptosis due to relaxation and atrophy of belly wall. Hornet's 

nest belly. 

In many cases of dilatation of the stomach, or of enteroptosis, the 
use of " Glenard's belt sign" may be resorted to. This consists in 
standing behind the patient, placing the hands upon the lower part of 
the abdomen and lifting upward and backward, when if gastroptosis 
or enteroptosis is present relief from the sense of dragging may be 
felt. 

I have found this method of diagnosis very serviceable. 

Gastric dilatation is often associated with atrophy of the gastric 



TEST FOR LACTIC ACID 299 

tubules, or at least an absence of any secretion of normal gastric 
juice. The matters vomited or washed out of the stomach are 
often devoid of hydrochloric acid, but loaded with an excess of 
lactic acid. 

Test for Lactic Acid. — Lactic acid is tested for as follows, the 
hydrochloric-acid test being given below: a few drops of neutral 
ferric chloride solution arc mixed with one or two drops of pure 
carbolic acid, 10 c.c. of a 5 per cent, solution of carbolic acid, and 
water added until an amethyst hue develops. A few drops of the 
filtrate derived from the stomach contents are now added, and if 
lactic acid or lactates are present the amethyst hue will become 
yellow in color. This is a very delicate test for lactic acid. 

Test for HC1. — The presence or absence of hydrochloric acid is 
determined in the following manner: The patient is directed to take 
no food for at least twelve hours before presenting himself to the 
physician. On his arrival for examination he is given what is 
known as "Ewald's test breakfast, ' which consists of an ordinary 
dry roll and a little over a half pint of water which lias been 
warmed, and he is directed, after swallowing these materials, to 
wait an hour. The stomach is now emptied by the introduction of 
the bulbed stomach tube, and the gastric contents filtered. A few 
minims of a solution of phloroglucin and vanillin are next placed in 
a porcelain dish and a few drops of the gastric liquid arc allowed 
to trickle down to the edge of the solution. The dish is gently 
heated over a spirit lamp or Bunsen burner, and if hydrochloric 
acid is present there will appear a red tinge. This is an absolute 
proof of the presence of hydrochloric acid. 

The solution of phloroglucin and vanillin is made as follows: 

Phloroglucin gr. xxx. 

Vanillin gr. xv. 

Absolute alcohol f 5j 

This solution is pale yellow in hue. It must be kept in dark 
bottles, as on exposure to the air and light it becomes brown and 
worthless. 

In some cases symptoms of gastric dilatation may arise from the 
presence of " hour-glass stomach" a state in which a stricture divides 
this organ more or less completely into two parts. The presence of 
this state may be determined by filling the stomach with water or 
gas from the halves of a Seidlitz powder taken separately. On per- 
cussion it will be found that the cardiac area is distended but the 
pyloric area is empty, and some minutes later the pyloric portion 
becomes distended. During this period the use of a stethoscope over 
the middle area of the stomach may reveal the sounds made by the 
passing of the fluid or gas through the stricture. If the stomach is 



300 



THE ABDOMEN AND THE ABDOMINAL VISCERA 



washed out by lavage until the liquid is clear and then after a short 
time washed again and the returned liquid is found to be foul, this 
is a sign of hour-glass stomach because the cardiac area has been 
filled by retained contents on the pyloric side of the stricture. So 
too the gastrodiaphane may reveal light only in the cardiac area. 




Fig. 120.— Hour-glass stomach. 

The Liver. — Normally, in the adult, this gland cannot be felt below 
the ribs, except part of the left lobe in the epigastrium occasionally. 
Sometimes, on deep inspiration, the diaphragm pushes the liver low 
enough to be felt. In children the liver is naturally large enough to 
be felt below the ribs. 

When the normal liver is percussed we find that it lies in the area 
shown in Fig. 115, and that as we percuss above it on the ribs in the 
mammary line we first get pulmonary resonance; then a little 
below this, impaired resonance, due to the fact that the lower edge of 
the lung is interposed between the chest wall and the liver; and 
still lower we find absolute dulness or flatness, due to the solid liver 
itself. Below this area, which ceases just below the lowest rib, we 
usually find tympany on percussion, due to the gas-distended bowel. 
If we percuss in the midsternal line, we get the same signs; but they 
begin as high as the nipple, or above it, and then cease at a line 
drawn across the abdomen about midway between the ensiform 
cartilage and umbilicus. To the left of the middle line of the ster- 
num the liver dulness merges into the cardiac dulness (Fig. 121). 
In the mammary line liver dulness begins at the fifth rib, laterally 
it begins at the seventh and eighth, posteriorly at the tenth rib, 
owing to the sloping of the diaphragm. 

When a hard and firm mass with a smooth surface can be felt in the 
right hypochondrium or right umbilical area, which is movable, and 



Tin-: li\ er 



301 



which has an edge which can be readily fell on deep palpation, 
particularly when the patient takes a long-drawn, deep breath, the 

mass is probably an enlarged liver or a liver pushed down into the 
abdominal cavity by a large pleural effusion, pneumothorax, a sub- 
phrenic abscess, or sometimes by an emphysematous lung. The 
causes of enlargement are lymphadenoma and amyloid degeneration, 
congestion, hypertrophic cirrhosis, abscess, carcinoma, sarcoma. 
When the surface is found to be smooth, the condition is probably 
amyloid or fatty degeneration, or congestion. If the surface is 




Fig. 121. — Showing percussion dulness of liver and heart. The outside line shows the area 
of partial dulness of heart and liver, modified by lung. The solid area is that of true hepatic 
dulness. At x, Traube's semilunar space. 

rough, it will probably be due to cirrhosis, which gives a granular 
sensation to the hand when the abdominal wall is moved over the 
organ. In malignant growth large and small nodules may often be 
found, and depressions or umbilications of its surface may be marked, 
but it must be remembered that cancer of the liver is not necessarily 
associated with the presence of nodular masses. On the contrary, 
the growth or growths may be large, yet project so slightly above the 
hepatic surface that they cannot be felt. In such cases there may be 
pain, marked emaciation, cachexia, and the organ be found much 
enlarged. 



302 THE ABDOMEN AND THE ABDOMINAL VISCERA 

The physician who feels distinct nodules on the surface of the liver 
should not immediately conclude that these are necessarily carcino- 
matous, for syphilis often produces a very extraordinary nodulation 
of the surface of this organ. So great is this, that when nodulation 
is excessive the possibility of syphilis being the cause is to be con- 
sidered. This form of disease is, however, rarely accompanied by 
as great hepatic enlargement as is that due to cancer with marked 
and multiple nodules. 

The consistency of the liver is usually very hard in cases of cirrho- 
sis, carcinoma, and amyloid degeneration. In cirrhosis there will be 
some ascites in many cases, some swelling of the legs perhaps, and 
dull pain in the hepatic region. The digestion will be disordered, 
there will be marked loss of flesh, and often hematemesis. Some- 
times*coma comes on. In the case of amyloid liver there will be 
a history of prolonged suppuration elsewhere, and there will be 
present disordered digestion, irregular bowel movements, and little 
pain. 

Marked tenderness of the hypochondrium is usually found in 
congestion of the liver, in inflammation of its tissues, such as that 
caused by an infection or by gallstones in its substance, and in malig- 
nant growth. Tenderness is practically absent in amyloid liver and 
in fatty degeneration. 

In cases of cirrhosis of the liver, whether it be in the hypertrophic 
or atrophic form, the patient rarely complains of the organ, and no 
symptoms which seem to him hepatic in origin may be present, save 
that in the hypertrophic state its size is increased, so that it can be 
felt below the ribs, whereas in the atrophic state it cannot be felt 
except by pushing the fingers well up under the ribs. The symptoms 
accompanying cirrhosis are chiefly connected with disorders of the 
alimentary canal, either through direct failure in the digestion and 
assimilation of food, or from changes in the blood supply of the 
abdominal contents. The following excellent diagram, from Sey- 
mour Taylor's Index of Medicine, shows what these symptoms are, 
and discovers their cause at a glance, the cirrhotic process, of course, 
obstructing the flow of blood in the liver (Fig. 122). It is a note- 
worthy fact that in the atrophic form jaundice is rare even in the 
very last stages of the disease, whereas in the hypertrophic form it is 
commonly met with. Ascites is common in the atrophic form, rare 
in the hypertrophic variety. 

Sometimes enlargement of the liver and ascites are due to adhesive 
pericarditis. The diagnostic signs of adhesive pericarditis consist in 
systolic retraction of the intercostal spaces in the anterior axillary 
line, and posteriorly at about the fifth or sixth rib on the left side, 
which retraction is followed by a diastolic rebound. If the patient is 
told to forcibly inspire or expire, the natural change in the position 



HEPATIC ABSCESS 



of the apex bea< of the heart in relation to the chest wall does not 
occur, neither does the edge of the lung on full inspiration diminish 
the area of cardiac dulness as it does in health. Pericarditis with 
ascites is often associated with hyperplastic perihepatitis, the "Iced 
Liver" of ( lurschmann. 

The physician who finds the lower margin of the liver abnormally 
low down in the abdominal cavity should not make a diagnosis of 
enlargement of this organ until he has assured himself that the exten- 
sion of the margin of the liver is not due to an effusion in the right 
pleural cavity which presses upon this organ. So, too, if the patient 
is a woman, the lower border of the liver may have been pushed 
down by tight lacing, and careful palpation may reveal a furrow 
across its surface produced by the corset. The displaced lower 

Morning Sickness 
Ha hint, 
Dyspepsia 



[Pall. 

Spleens and 

uSnlargt nu nl 





Ha niorrhoids 

Fig. 122.— To illustrate Bymptoma of cirrho6is of liver. (Seymour Taj 

border of the gland gives rise to the diagnosis of enlargement of the 
liver if careful percussion shows that the upper border of liver dulness 
is in its normal place. If the upper border of the liver is depressed, 
and pleural effusion is absent, it is a sign of floating liver. 

Hepatic Abscess. — When, on palpating the liver, we find marked 
tenderness and some swelling, and. associated with these symptoms, 
fever, rigors, sweats, and sometimes vomiting, and, in addition, a 
history that the patient has had dysentery or has had exposure to 
tropical heat or has swallowed bad water, the presence of an 
abscess of the liver is indicated. This may be single or multiple. 
If the latter, it is probably due to pyemia, and no spot of fluctua- 
tion will be found, as a rule; whereas, if it is laro-e and single, 
fluctuation is sometimes felt. Further, the enlargement of the liver 
in the pyemic form is uniform, whereas in the single abscess there is 



304 THE ABDOMEN AND THE ABDOMINAL VISCERA 

often one spot which is swollen or enlarged. The history of the case 
will usually separate the conditions, one from the other, for diag- 
nostic purposes, for in the case of abscess the history will probably 
be that of a person exposed to tropical heat or one who has had 
an injury, an acute infection, or an amebic dysentery. More rarely 
a single hepatic swelling may be due to hydatid cyst, but the history 
and presence of fluctuation, combined with the result of examining 
the fluid aspirated from the swelling, will decide the diagnosis. 
Further than this, hydatid cyst yields on percussion a peculiar 
vibratory thrill called the hydatid thrill. Three fingers are placed 
over the area, the middle one being pressed firmly upon the growth 
and the lateral ones but lightly. The middle finger is now percussed 
with the other hand and allowed to remain in situ, when an after- 
thrill may be felt in the other fingers. 

Pancreatitis. — The appearance of sudden swelling in the neigh- 
borhood of the pancreas, associated with intense pain, nausea, and 
vomiting, may be due either to acute hemorrhagic pancreatitis, to 
hemorrhagic infarction of the intestine, to intestinal obstruction, 
acute cholecystitis, or to acute peritonitis resulting from perforation 
of the stomach. (See chapter on Pain.) The last three are the 
more common. An exploratory operation is the only way of decid- 
ing the diagnosis positively, although the history of the patient may 
aid us in deciding the cause of the illness. Thus, if there is a 
history of gallstone colic, this may indicate that a stone has become 
impacted in the common duct near the papilla. Such an accident, 
if it dams back the secretion into the pancreas, causes hemorrhagic 
pancreatitis with fat necrosis. Sometimes, however, the symptoms 
of hemorrhagic pancreatitis are more prolonged, and life lasts for 
several weeks, local swelling, jaundice, and pain being present, with 
symptoms of suppuration. 

Pancreatic Cysts. — Very rarely swelling in the epigastric region, 
either rapid or slow in onset, follows upon the formation of cysts in 
the pancreas, as a result of obstruction of a duct of the gland. 
When they occur, these cysts may quite fill the abdominal cavity, 
although, as a rule, they are small. 

Hemorrhage into the Lesser Peritoneum. — As pointed out, however, 
by Jordan, the cause of a swelling in the pancreatic region may be 
hemorrhage into the lesser peritoneal cavity. He summarizes some 
of his views in regard to this matter as follows : 

" Contusions of the upper part of the abdomen may be followed 
by the development of a tumor in the epigastric, umbilical, and left 
hypochondriac regions. Such tumors may be due to fluid accumu- 
lating in the lesser peritoneal cavity, and when the contents are 
found (on aspiration) to have the power of converting starch into 
sugar we may assume that the pancreas has been injured." Finally, 



EPIGASTRIC PULSATION 



305 



Jordan states that "many such tumors have been regarded as true 
retention cysts of the pancreas." 

Pyopneumothorax Subphrenicus. — In other instances a swelling in 
this neighborhood may be due to what is called pyopneumothorax 
subphrenicus, a condition of abscess in the peritoneal cavity below 
the diaphragm, produced by perforation of the stomach or transverse 
colon or appendicitis. The abscess so produced may contain gas, 
and for this reason the swelling may be quite resonant on percus- 
sion (Fig. 123). Abscess in this region also follows abscess of the 
pancreas or fat necrosis of this organ in rare instances. 



Compressed 

lunrj 



t__A]» X b- fit 

not greattt 

displaced. 




Fig. 123. —Left pyopneumothorax subphrenicus. (After Maydl.) 

Epigastric Pulsation. — Hither palpation or inspection may reveal 
pulsation in the epigastric area. This may be due to distention or 
enlargement of the right ventricle or to excessive aortic pulsation 
or to venous pulsation in the liver. If due to the action of the ven- 
tricle there will be additional signs of cardiac disturbance on exam- 
ining the heart, and in hepatic pulsation there will not only be 
found tricuspid regurgitation, but a pulsation below the floating ribs 
at the lower border of the liver. An excessive aortic pulsation is 
often met with in hysterical or neurasthenic persons without any 
abdominal lesion. Epigastric pulsation is also often transmitted 
from the aorta to the hand by enlarged abdominal glands or tumor 
masses. If the pulsation of the aorta is not transmitted by glands or 
tumors, impulse may be due to aneurysm of the abdominal aorta, 
the diagnosis of which is established if, in addition to a pulsating 
20 



306 THE ABDOMEN AND THE ABDOMINAL VISCERA 

sensation, we also find on palpation a marked thrill, an expansile 
movement of the tumor, and on auscultation we hear a bruit. Pain 
due to pressure of the aneurysmal sac upon some of the nerves of 
the abdominal cavity may also be a prominent symptom, but it 
should be remembered that aneurysm of the abdominal aorta is so 
rare that the law of probabilities is always against its presence. 
Sometimes a horseshoe kidney extending across the vertebral column 
will mislead one into a diagnosis of an intra-abdominal tumor, for 
horseshoe kidney is not very rare, being found as often as once in 
1650 autopsies. 

Tumors of the Bowel. — Tumors or foreign bodies in the bowel 
can nearly always be moved about unless bound down by inflam- 
matory adhesions, so differing from growths which involve the 
immovable parts, such as the retroperitoneal glands. Very rarely 
we find a cancerous tumor of the omentum, but when it is present 
it usually becomes retracted and indurated so that its hardened edges 
can be felt extending across the abdominal cavity. More commonly 
when multiple nodules are found in the omentum or studded over the 
surface of the bowels, they are due to peritoneal tuberculosis. Not 
rarely these nodular masses are also found studded over the mesentery. 

Localized masses due to other causes than those already dis- 
cussed are due to impaction of feces, volvulus and intestinal obstruc- 
tion from other causes, as, for example, cancer of the bowel. > Such a 
growth occurs most frequently in the cecum, when the tumor will 
be found in the right groin, or in the sigmoid flexure, when it will 
be found in the left groin. 

Floating Kidney. — Floating kidney may also cause a marked 
movable swelling or tumor-like mass in the upper zone of the 
abdomen. It may be mistaken for a tumor of the uterus, or of the 
liver, omentum, ovary, or spleen, or even for a much distended 
gall-bladder. If the belly walls are thin, the peculiar shape of the 
kidney can sometimes be outlined by palpation, and even the pul- 
sation of the renal artery can be felt; but, as a rule, this cannot be 
done, and the dilatation of the pelvis of the kidney by the obstruc- 
tion of the ureter, which has become twisted, may distort the shape 
of the organ. Deep palpation of the flank, if the kidney has floated 
away from its normal seat, may reveal lessened resistance in this 
area, and bimanual palpation, one hand being placed at the back 
and the other in front, may reveal the presence of the organ else- 
where. Further, if the patient be made to lie on the side, the dis- 
located kidney may sometimes be clearly outlined by bimanual 
palpation. In other instances, the patient lying on the back with 
the thighs flexed, the physician grasps the side between the rib 
and the iliac spine and directs the patient to take a full breath, 
when the kidney, if movable from its normal resting place, can be 



CYSTIC KIDNEY 307 

fell passing down between the thumb in front and the fingers 
behind. The fingers should be in the flank and the thumb over the 
side of the abdomen (Fig. 124). If the kidney be pressed upon 
gently, it can be slipped back into place on expiration. In other 
instances the patient stands erect, and the physician places the 
finger tips of the left hand in the lumbar region, and pressure is 
made toward the front of the body. The fingers of the right hand 
are placed anteriorly, and pressure is made backward and upward 
so as to engage the kidney between the finger tips of the two hands. 
The vertical posture of the body aids in displacing the kidney, which 
may stay in place in the dorsal decubitus. The kidney may slip with 
a jerk, if already displaced, back into its normal position; or. if 
already in place, it may be felt to escape downward into the abdomi- 
nal cavity. Pressure on a floating kidney causes a peculiar nauseat- 




Fig. 124. — Method of examining for floating kidney. The physician grasps the side with 
his hand in such a way that the fingers and thumh are approximated, and when the patient 
takes a full breath the kidney can be felt slipping through between the fingers and thumb. 

ing pain somewhat resembling that produced by squeezing a testicle, 
and when the organ is caught between the hands it slips from the 
pressure with a sensation resembling that felt by the fingers when an 
orange seed is pressed between the finger and thumb and escapes 
the pressure. The condition of floating kidney is more common in 
women than in men, but it occurs in both sexes. In (>(>7 cases, 583 
occurred in females and 84 in males. (Kuttner.) It is generally the 
right kidney which is displaced, although dislocation of the left 
kidney is not very rare. In Kuttner's 727 cases it occurred on the 
right side in 553, on the left in 81, and both sides in 93. Sometimes 
violent attacks of renal pain occur in cases of floating kidney. These 
have been called Dietl's crises. (See chapter on Pain.) 

Cystic Kidney. — When the kidney is enlarged from cystic degener- 
ation, from ordinary hydronephrosis, and from echinococcus cysts, 
it may be readilv felt in the umbilical area in many instances. 



308 



77/ A' ABDOMEN AND THE ABDOMINAL VISCERA 



Hydronephrosis. — Hydronephrosis has been mistaken, in children 
particularly, for sarcoma of the kidney, and in adult females for 
ovarian tumor. The diagnosis in some of these cases can be made 
only by tapping. The fluid obtained in hydronephrosis will usually 
be somewhat turbid and contain epithelial cells. It should not be 
forgotten that the condition of hydronephrosis may be intermittent, 
for, if this is not remembered, the physician may be misled into 
thinking that the disappearance of the swelling is due to a floating 




Fig. 125.— Method of examining for floating kidney. The physician grasps the side with his 
hand in such a way that the fingers and thumb are approximated, and when the patient takes 
a full breath the kidney can be felt slipping through between the fingers and thumb. 



kidney slipping back into its place. This intermittence in the size 
of the tumor may be of considerable diagnostic aid, for sudden 
decrease in size would indicate the escape of fluid through a tempo- 
rarily patulous ureter, and its redevelopment would indicate that 
this pathway of escape was again closed. Should the fluid escape 
into the bladder free urination would naturally take place shortly 
after the tumor decreased in size. Hydronephrosis may be bilateral. 
In 13 out of 20 cases collected by Roberts this was the case. 
Severe pain is often a symptom of intermittent hydronephrosis. 



THE SPLEEN 309 

Pyelonephritis and pyelonephrosis may closely simulate hydro- 
nephrosis, but fe/er and the presence of pus in the urine will aid in 
making the differential diagnosis. 

Bulging of the flank, with pain, fever, and perhaps fluctuation, 
indicates perinephritic abscess or caries of the spine with cold 
abscess. 

Mesenteric Cyst. — A fluctuating swelling in the epigastrium or 
flank may also arise from cysts of the mesentery. These may grow- 
to a very large size. In other cases a cystic hydroma of the tissues 
near the kidney may be present. Hawkins has recorded a case in 
which a large cyst, with an atrophic third kidney attached to it, 
filled nearly the entire right side of the belly, and from which after 
death five pints of clear fluid, devoid of albumin and casts, were 
removed. As already indicated, much diagnostic aid can often be 
given by tapping an obscure abdominal cyst. 

J. (r. Clark has recommended a method of separating solid from 
fluid tumors, which is called trhnanual percussion. This consists 
in fixing the mass between two hands, one below it if possible, the 
other above it. An assistant now percusses, striking the finger of 
the physician. By this means a thrill can be felt which would 
otherwise be lost. 

Phantom Tumor. — "Phantom tumor" is generally found in hys- 
terical women, and often leads to ludicrous errors in diagnosis. It 
is due to persistent dilatation of a knuckle of intestine by gas, 
thereby forming a moderately hard and more or less constant mass, 
which may resemble a real tumor. Examination of the patient under 
ether will usually reveal its true character. This state is to be differ- 
entiated from what Nothnagel has called "intestinal rigidity." In 
this condition a knob projects through a thin anterior abdominal 
wall and gradually grows larger until in the course of a few 
moments it sinks out of sight and touch. It is a disorder of peris- 
talsis. Localized superficial and inconstant tumors may arise 
through spasmodic but localized contractions of the recti muscles. 

Umbilical Hernia. — Finally, a swelling in the neighborhood of the 
umbilicus should always arouse the suspicion of an umbilical 
hernia. The situation of the swelling at the umbilicus, the fact that 
percussion over it gives a highly tympanitic note, owing to the gas 
in the prolapsed gut, and the possibility of reducing its size by taxis 
in some cases, will render a diagnosis of umbilical hernia possible. 

The Spleen. — In the left hypochondrium the spleen can be very 
readily outlined by percussion in persons not inordinately fat. Its 
normal position is best shown in the aceompanving figure. i^See 
Fig. 126.) 

The upper border of the spleen is on a level with the tenth dorsal 
vertebra and the lower border on a level with the end of the eleventh 



310 THE ABDOMEN AND THE ABDOMINAL VISCERA 

rib. Its upper edge or limit is on a le\el with the ninth rib. In 
percussing the spleen heavy percussion is to be avoided, since this 
may develop the resonance of the stomach or bowels. The spleen 
cannot be palpated unless greatly enlarged, but it may be found 
bulging from beneath the lowest rib in typhoid fever; in scarlet 
fever; as the result of acute or chronic malarial fever; in leukocy- 
themia of the splenomedullary variety (see Fig. 128) (see chapter 
on the Blood); in amyloid disease, as that after long suppuration; in 
early syphilitic infection; and in any disease which causes venous 




Fjg. 126 — Normal position of the spleen. 

engorgement of the abdominal viscera, such as cardiac disease or 
hepatic cirrhosis. The spleen sometimes reaches a very large size 
in the disease which has been called "splenic anemia." In this con- 
dition we have a state resembling Hodgkin's disease, save that there 
is not the involvement of the lymphatic glands. The blood, unlike 
that in true leukemia, does not show great changes in the white cells, 
any changes present consisting in an increase in the relative number 
of the lymphocytes, which may, in some cases, make up nearly all of 
the leukocytes. The red cells are greatly decreased in number, and 
there are present poikilocytes, megalocytes, and microcytes. Closely 
allied to this condition of the spleen is that which consists in the so- 
called " Band's disease," in which the spleen is also greatly enlarged. 
This disease is divided by Banti into three stages : a stage of anemia 



THE SPLEEN 



311 



characterized by enlargement of the spleen, and lasting from three 
to ten years; a transitional stage; and a third stage of marked ascites, 
which usually terminates in a few months. In some cases of so-called 
Banti's disease, hemorrhages take place, such as vomiting of blood; 
nose-bleed, hemoptysis, and hematuria. Banti's disease differs from 
splenomedullary leukemia in the absence of an excess of white cells, 
and it is supposed to differ from splenic anemia in that there is not 
the same increase of lymphocytes as is characteristic of that condi- 









Fig. 1.7. — A case nl chronic enlargement of the spleen following typhoid fever. The dark 
line shows the margin of the organ on palpation, while the retraction in the line and the 
dotted line indicate the position of the splenic notch. (From the author's wards in the Jeffer- 
son Medical College Hospital.) 



tion. It is to be remembered that splenic anemia and Banti's disease 
are scarcely regarded as pathological entities by many clinicians. 
These terms cover obscure conditions about which we know little. 
(For splenomegaly with polycythemia, see chapter on the Blood.) 

Sometimes displacement of the spleen downward arises from 
emphysema of the lungs or left-sided pleural effusion. 

Acute splenic swelling sometimes comes on in cases of general 
septicemia. 



312 



THE ABDOMEN AND THE ABDOMINAL VISCERA 



Nearly always the splenic surface is smooth, except for the notch 
in its surface, unless the disease be the rare condition of hydatid 
disease or carcinoma. 

In connection with the subject of abdominal tumors, we should 
not forget the possibility of a floating spleen, a rare condition, but 
one more common than is generally thought. The shape of the 
organ, if it can be palpated, will aid the diagnosis, and the pres- 




Fig. 128. 



-A case of enormous enlargement of the spleen in splenic leukemia. 
(From a private patient.) 



ence of resonance on percussion over the area of normal splenic dul- 
ness will confirm the diagnosis that the spleen has become displaced. 
As the spleen in this condition may fall as low as the virgin uterus, 
it may simulate any growth from a uterine myoma to a tumor of the 
bowel or pancreas. By reason of twisting of its pedicle and second- 
ary engorgement, its size may be enormous; but if this condition 
continues, atrophy finally takes place. As such a dislocated spleen 
drags on the stomach and pancreas, it may cause a long train of 



THE GROINS 313 

curious symptoms, and even intestinal obstruction. Sutton asserts 
that by pressure it may cause displacements of the uterus. 

In cases in which it is difficult to determine the location of an 
abdominal growth it may sometimes be localized by distending the 
colon with air, which is gently injected into the bowel by an ordinary 
bulb syringe. 

The Groins. — There yet remains for discussion the significance 
of increased resistance on palpation, and percussion dulncss, in the 
groins. 

In the right iliac region the presence of swelling, increased resist- 
ance, impaired resonance, or tympanites, particularly if pain and 
tenderness are present, point strongly to appendicitis or to inflam- 
mation about the caput coli. Sometimes, however, the presence of a 
distinct lump in this region in a person advanced in life may mean a 
malignant growth, for carcinoma of the caput coli is not rare. 

If the left groin is affected in a person well advanced in years, 
carcinoma is also to be regarded as possible, for the sigmoid flexure 
is a frequent seat of such growths. In a young person or a child 
impaction of feces, a foreign body, or intestinal obstruction is also 
to be considered. (See chapters on Vomiting and on the Bowels.) 

For the diagnosis of renal disease reference is to be made to the 
chapters on the Bladder and Urine, the Blood, the Bloodvessels and 
the Pulse, and upon the Thorax (that part on the Heart), to the 
chapters on Vomiting and on Headache, and to those on Coma and 
Unconsciousness, and Convulsions and Spasms. 

For further information in regard to the diagnosis of diseases of 
the abdominal viscera, the reader is referred to the chapter on the 
Skin (that part on Jaundice), the chapter on Vomiting (that part 
on Intestinal Obstruction), to that on the Bladder and Urine, and 
to that on the Bowels and Feces. 



CHAPTER X. 

THE BOWELS AND FECES. 1 

Constipation and diarrhea — The cause of these two symptoms and their diag- 
nosis — The diseases in which these symptoms occur — Choleraic diarrhea — 
Dysentery — The color of the feces — Intestinal parasites. 

The consideration of the condition of the bowels and feces as 
indicative of disease affecting the intestines themselves and other 
organs closely associated with their functions, can be best divided 
into several parts, namely, the functional disorders of the intestines 
and the organic diseases from which they may suffer, on the one 
hand, and the appearance of the feces in both functional and organic 
diseases of the abdominal viscera in general, on the other. The most 
common forms of intestinal disturbance are constipation and diarrhea. 

Constipation. — Constipation may be due to mere sluggishness of 
bowel movement because of both nervous and muscular atony, or to 
deficient secretion of the intestinal juices, or, again, to the too rapid 
absorption of the liquids from the fecal matter while it is passing 
through the colon. It is also associated with all those conditions 
which prevent the proper flow of bile, which liquid very materially 
increases peristalsis. Thus, we see obstinate constipation in most 
cases of true jaundice; in cases of hepatic disease, producing a defi- 
cient biliary flow; and in phosphorus poisoning, in which the fatty 
degeneration and hepatitis prevent biliary secretion. Further than 
this, the constant ingestion of foods which are absorbed nearly in 
toto, or, in other words, leave little residue, particularly raw or boiled 
milk, produces constipation. Again, the use of wines containing 
large amounts of tannic acid may produce similar results because of 
the astringency of this substance, and chronic constipation from the 
use of large quantities of badly infused or boiled tea made with hard 
water is frequently met with. 

When the feces are very dry, the cause may be lack of liquid 
ingested, and the remedy be full draughts of pure water; or, 
again, constipation occurs as a manifestation of diabetes insip- 
idus or diabetes mellitus, because the polyuria characteristic of 
these affections drains the body of liquid. Obstinate constipation 
should, therefore, always call the physician's attention to these 
affections and to two other possibilities, namely, that the con- 

1 For intestinal obstruction in its various forms, see chapter on Vomiting. 



DIARRHEA 315 

dil ion depends upon wilful disregard by the patient of the calls of 
nature, so that the bowel is forced to retain fecal matter until it 
becomes hard and dry; or, quite as important, that the constipation 
may be due to some reflex cause, which, as the result of irritation, 
results in an arrest of peristaltic movement. Thus, a woman with 
ovarian and other pelvic trouble may have obstinate constipation 
which yields little, if at all, to purgatives, but readily to nervous 
sedatives or even to an opiate. Or, again, in chronic lead poison- 
in (j the inhibitory fibers of the splanchnic nerves and the intestinal 
muscularis may be so irritated that peristalsis is impossible. Here a 
hypodermic injection of morphine may make a movement possible. 

The organic diseases of the bowel producing constipation are many 
and of great importance. They consist in intestinal obstruction in 
all its forms, as by bands, growths, by the process of intussusception, 
by volvulus, by cicatricial contractions, and by impacted foreign 
bodies or fecal matter. The presence of a sudden attack of consti- 
pation, or the presence of this condition in a degree which fails to 
yield to mild laxatives, should always put the physician on his guard 
lest some grave condition is present. As severe and, finally, sterco- 
raceous vomiting is a fairly constant and more marked symptom of 
intestinal obstruction than is constipation, a discussion of the various 
symptoms of intestinal obstruction will be found in the chapter on 
Vomiting, and the diagnosis of growths of the intestine will be found 
in the chapter on the Abdomen. 

Aside from these causes, it is manifestly impossible to discuss all 
the conditions of the system in which constipation may be present. 
The physician must always bear in mind that constipation often 
results in the absorption of poisonous materials from the bowels, 
which in turn may produce all sorts of symptoms, nervous or other- 
wise, from epileptiform attacks, in rare cases, to severe headache and 
vertigo, with vomiting, in others. 

Diarrhea. — Diarrhea of an acute type depends, as a rule, upon one 
of four causes, namely, the presence of irritant material in the bowel, 
which the intestines attempt to get rid of by increased secretion and 
excessive peristalsis; relaxation of the bloodvessels of the intestine, 
with profuse serous leakage and consequent watery purging; acute 
inflammation, with excessive secretion of mucus; and the endeavor 
of the system to eliminate poisons in this manner, as in cases of 
sudden profuse diarrhea, in cases of chronic rctial disease, in which 
the purging is an effort at elimination. The last-named forms of 
diarrhea are usually sudden in onset and speedily get well of them- 
selves, and it is a mistake to check them too suddenly. 

It is impossible to speak of all the possible causes of diarrhea, or 
of all the diseases in which it is met with. Only those in which it is 
a prominent symptom, or one of importance, can be discussed. 



316 THE BOWELS AND FECES 

One of these is cholera morbus, a disease which manifests itself 
in profuse watery purging, accompanied by violent pain in the belly, 
and, after several stools have passed, in a considerable amount of 
tenesmus. Mucus is almost entirely absent from the dejecta, but 
particles of undigested food may be found in them. Vomiting is 
often a severe and simultaneous manifestation of the gastrointes- 
tinal disorder which exists, and, if the attack be very severe, it is 
practically impossible to separate it from true cholera Asiatica if an 
epidemic of that disease is present. The patient speedily becomes 
cold and pinched-looking, exceedingly weak, and finally may pass 
into collapse. The pulse becomes feeble, rapid, and running; the 
face livid, and finally the patient may develop the fades Hippo- 
cratica. The urine is greatly decreased or entirely suppressed, 
because of the watery purging, and possibly by reason of the effects 
of certain poisons upon the kidneys. In the great majority of cases 
the symptoms are not so severe as this, and complete recovery ensues 
as soon as the offending materials are passed out of the bowels and 
the patient has time to convalesce. 

When an attack of diarrhea, such as has just been described, 
comes on in a young child it is usually called cholera infantum, or 
"summer complaint," and it is nearly always due to improper feeding 
or to the unintentional use of bad food or bad milk. The stools of 
the child are usually at first filled with curds of milk and green masses, 
looking as if the curds had been stained with grass juice or spinach. 
The child often passes with extraordinary rapidity into a state of 
collapse, and may die in a few hours or days. The tenesmus often 
becomes constant and is a distressing symptom, and the tissues 
become shrunken to a marked degree. The child manifests not only 
the evidences of the results of profuse purgation, but, in addition, 
is evidently intoxicated by the toxins absorbed from the bowel, so 
that it lies on the lap of the nurse in a relaxed and torpid state. The 
surface of its body is often abnormally cold, and its extremities may 
be pinched and blue; but the temperature of the internal organs is 
generally abnormally high, so that while the axillary temperature 
may be below normal, the thermometer will reveal a temperature of 
from 102° to 103° in the rectum. Sometimes the head becomes 
retracted, as if meningitis was present. The respirations may be 
sighing or of the Cheyne-Stokes type. 

If the child or adult is seized with symptoms such as those described 
under cholera morbus or cholera infantum, and a suspicion of the 
presence of true cholera is raised, Are there any facts which will point 
to the correct decision in a case, even if, as already stated, a positive 
differential diagnosis cannot be made? In the first place, a train of 
symptoms of a malignant type points to the true cholera, rather than 
cholera morbus, or cholera nostras, as it is sometimes called. Again, 



DIARRHEA 317 

the evidences of infection or general systemic disease indicate the 
epidemic malady rather than does a profuse diarrhea alone. Thus, 
the systemic signs of infection may be so great that death from infec- 
tion in true cholera occurs before diarrhea even begins. Again, it 
would be possible to determine the presence of true cholera if the 
comma bacillus could be demonstrated; but this requires the exami- 
nation of the fecal matter to be made by an expert who is familiar 
with the technique of examining fecal matter for the germs and with 
the necessary measures for their artificial culture. 

Symptoms identical with the more violent forms of cholera nostras 
or true cholera may be produced by acute poisoning by antimony, 
except that in this case we often have profuse sweating and saliva- 
tion early in the attack. The same symptoms of vomiting, purging 
of rice-water stools, collapse, cramps in the calves of the legs, and 
violent pain in the abdomen may be present. A differential diag- 
nosis without the history of the patient having taken poison is Impos- 
sible, except by a chemical analysis of the vomited matter, which 
will contain antimony, as will the stools and the urine. The utmost 
care should be used that the vessels which receive these materials 
are chemically clean, that they are hermetically scaled until ready 
for the expert analysis, and that they are in the hands of thoroughly 
responsible parties up to the date of analysis. 

While arsenic may cause somewhat similar symptoms to those due 
to antimony, the stools are generally bloody. Rarely certain 
poisonous toadstools produce somewhat similar symptoms. 

If an adult who has not eaten anything which could have 
produced a diarrhea, as, for example, bad food, is seized with 
profuse watery purging, with very little or no pain, and without 
nausea and vomiting, it is probable that he is suffering from the acute 
nervous diarrhea which sometimes results from exposure to severe 
nervous strain. To illustrate the character of these cases the author 
may mention the fact that it is quite common for him to see medical 
students, exhausted by a long winter's work and anxious about their 
examinations, seized by an attack of profuse watery purging in the 
middle of the night preceding the examination of which they stand 
most in dread. 

In other cases profuse purging develops suddenly in hot weather 
as a form of heat prostration. 

Care must be taken by the physician in all cases of sudden and 
profuse diarrhea to which he is called to exclude the presence of 
renal disease, for purging may be an effort at elimination of effete 
materials, and its sudden arrest by drugs may induce uremic con- 
vulsions or coma. 

Sudden attacks of profuse watery diarrhea in which the patient 
passes great quantities of liquid from the bowel, with or without pain 



318 THE BOWELS AND FECES 

in association therewith, may be due to locomotor ataxia, manifesting 
itself in an "intestinal crisis." 

In cases of persistent or obstinate diarrhea, serous or catarrhal, 
in which there is an excessive peristalsis which hurries the intestinal 
contents along so fast that the food cannot be properly digested, the 
physician should remember that fissure of the anus or some other 
source of irritation may be present in the lower bowel which produces 
reflex excitability of the nerves governing the bowel movements. 
In other cases a stricture in a feeble, dilated rectum will cause reten- 
tion of feces until irritation, tenesmus, and even loose mucous move- 
ments are produced. 

If, instead of watery or serous movements, the patient is attacked 
by a more or less acute diarrhea, accompanied by great pain and 
distention of the belly, and if there is marked tenderness on pressure 
over the transverse colon and mucus in the feces, which are not in 
very large quantities after the first few movements, there is probably 
present the condition known as enterocolitis, or inflammation of the 
ileum and colon. It is met with in both children and adults, and 
differs in its course from cholera morbus and cholera infantum very 
markedly. The pain is usually more constant, more aching, and less 
griping in character. Vomiting is not a constant feature, as it is in 
the watery choleraic diarrheas, and the course is more subacute, 
the duration of the illness usually being from one to three weeks. 
If food which is difficult of digestion has been eaten, it is passed, 
still undigested, from the bowel, and is apt to be coated with mucus. 
Such a diarrhea is called lienteric diarrhea. 

Not far removed from this type of cases are those of a more chronic 
character depending upon more grave and lasting alterations in the 
gastro-intestinal mucosa. As a rule, the greater part of the trouble 
exists in the colon, and more or less griping pain in the neighborhood, 
namely in the upper umbilical area and left groin, may be present 
before each movement. The abdomen is apt to be distended and 
quite tender on pressure, particularly in varying spots, and consider- 
able loss of bodily weight is apt to ensue, chiefly from failure on the 
part of the digestive tube to absorb the food that is eaten. The 
movements are not markedly watery, but are usually unformed and 
about the consistency of oatmeal gruel or a little thicker. Flakes of 
mucus are often found in large amounts in the fecal matter, and the 
feces may be frothy or flaky as the result of fermentation. Blood and 
pus are very rarely seen in the movements of these cases, unless the 
blood escapes from an inflamed hemorrhoid. Sometimes, when 
these cases are very severe in character, the mucus takes the shape 
of long cord-like or worm-like strings, or even seems to be mem- 
branous in character, the so-called mucomembranous enteritis. In 
other instances the feces, when formed, are passed in ribbon- 



DIARRHEA 319 

shaped masses, duo either to spasm of the muscular fibers 
of part of the lower bowel or to cicatricial contractions from 
the healing of old ulcerations. In very severe cases the condi- 
tion of the intestines gradually advances from a mild follicular 
enterocolitis to one of actual deep ulceration, and under these cir- 
cumstances blood and pus may be present in the movements. At 
such times the pain produced by the patient having a movement of 
the bowels, or by the passage of fecal matter over the ulcerated sur- 
face, may be intense, and the invalid will often state that the pain 
feels as if one spot in the gut were made more painful by the feces 
rubbing over it. Such cases often continue for years, while some of 
them ultimately get well, others become chronic invalids from the 
slow changes in the intestinal walls. In this connection the diarrhea 
of tuberculosis is not to be forgotten, depending, as it does, either 
upon the general infection or upon the development of ulcerations 
in the intestinal canal. 

In some cases in which the patient after exposure to cold or wet 
is seized with violent pain in the epigastrium and a feeling of weight 
in the rectum, a few loose movements and then intense tenesmus 
and bearing-down, with only a few drops of mucus in the way of a 
movement, the condition is one of acute rectal catarrh or proctitis. 

The cases just named in the preceding paragraphs are to be sepa- 
rated from those in which there is true dysentery. Dysentery is a 
term very loosely applied, by the laity in particular, to any form of 
severe diarrhea, particularly if there are blood and mucus in the 
movement. In reality the term dysentery should be limited to cases 
due to an infection, and very apt to occur in epidemics. 

Let us suppose that a patient is seized with diarrhea and some 
pain in the belly, and with only a slight chill, or this symptom may 
not be present. The pain soon becomes more and more colicky, and 
the stools are passed with ever-increasing bearing-down or tenesmus. 
The effort to empty the bowel, after it is in reality thoroughly 
emptied, results in agonizing bearing-down pains. Fever to the 
extent of from one to three degrees may be present. Thirst is exces- 
sive, the stomach is usually retentive, and the stools are first the 
ordinary bowel contents, and then mucus, which may be blood- 
streaked. Soon the mucus becomes jelly-like in appearance and more 
thick and tenacious, and, finally, after several days it begins to look 
mucopurulent, and the stools are less frequent. Sometimes small, 
bullet-like, hard pieces of fecal matter are shot out of the rectum 
after severe straining. Recovery usually begins at from seven to ten 
days. The entire trouble seems to be in the large bowel, and par- 
ticularly in the sigmoid flexure and rectum. Such are the symptoms 
of ordinary mild dysentery of hot climates or of summer weather in 
the temperate zone. 



320 THE BOWELS AND FECES 

The severity of the disease is much greater in hot weather, 
and the prognosis is not good in severe cases coming on during 
an epidemic. 

On the other hand, if the patient has an irregular diarrhea after 
or during a residence in tropical parts, which may or may not have 
a sudden onset, with moderate fever and considerable loss of flesh, 
and has moderate bellyache, which soon becomes much less, and if 
the stools as just described above become more and more fluid, and 
the diarrhea intermits, the physician should think of the case being 
probably one of so-called amebic dysentery, a condition of infection 
by the so-called ameba coli. The course of the disease is slow, 
lasting from six to twelve weeks, and the death rate is high. Con- 
valescence is always very slow, and liver abscess due to an hepatic 
infection by the ameba coli is very frequent. Sometimes secondary 
abscess of the lung develops. 

A positive diagnosis of this variety of dysentery is made by the 
discovery of the amebse in stools. These microorganisms possess 
active ameboid movements and are found in greater number when 
the diarrhea is severe. They are to be sought for in the small gelat- 
inous masses which are found in the feces. Sometimes the entire 
stool seems loaded with amebaB; at other times only a most careful 
search will discover them. They are more refractive than the cells 
found in the feces, and contain numerous vacuoles, so numerous in 
some cases that the cells look very granular. These must not be 
mistaken for the compound granular bodies found in the feces. 
When they are active a division into an endosarc and an ectosarc 
can be discovered. Often red blood cells will be found in the amebse. 

Epidemic dysentery is usually due to Shiga's bacillus. 

Sometimes a diphtheritic or pseudomembranous dysentery is devel- 
oped in persons having chronic heart disease, and it has been seen as 
a sequel of acute croupous pneumonia. This is called secondary 
diphtheritic dysentery, and death generally results from exhaustion, 
only a suspicion of the intestinal condition having existed during 
life. Such a state is sometimes a complication of Bright's disease, 
probably owing to the irritation of the intestinal mucous membrane 
produced by the urea decomposing into the carbonate of ammonium. 
In acute primary dysentery of a diphtheritic character the patient may 
rapidly pass into a typhoid state, and the case be diagnosticated as 
one of typhoid fever with profuse diarrhea. The discharges are the 
only means of separating the two conditions (enteric fever and diph- 
theritic dysentery), as they often are filled with blood and mucus in 
dysentery, a condition rarely seen in typhoid fever. 

Dysentery may be confused with the diarrhea sometimes produced 
by a malignant and ulcerating growth in the sigmoid flexure or rectum, 
but a physical examination will usually reveal the tumor, and the 



THE FECES 32] 

cachexia will aid in pointing to it as the cause. Syphilitic ulceration 
of these pails may cause a somewhat similar train of symptoms. 

Again, it is by no means rare to meet with the passage of several 
mucopurulent movements each day in persons who have pulmonary 
gangrene or pulmonary tuberculosis, partly due to the swallowing 
of fetid sputum or tuberculous ulcer at ion of the bowels. 

Diarrhea is also a symptom of septicemia. Distantly allied to this 
form of diarrhea is that seen in persons who have dissected a 
putrid body ("dissecting-room diarrhea," so called). 

Finally, it is interesting to note that paroxysmal attacks of -em- 
mucous or bloody diarrhea sometimes come on in cases of exophthal- 
mic goitre. Diarrhea of a more or less severe type may come on in 
cases of hysteria, often associated with tremendous eructation- of 
gas and rumbling in the stomach and bowels. 

Fatty diarrhea may ensue if feeble persons already suffering from 
irritable bowels take an excess of cod-liver oil, and in some cases it 
possesses great diagnostic importance. If associated with diabetes, 
it gives us reason to believe that there is disease of the pancreas 
producing both the glycosuria and the lack of digestion of the fats. 
Sometimes in jaundice, however, fat is found in the stool- owing to 
the lack of bile to emulsify it in the intestine. 

The Feces. — In this connection we naturally pass on to a discus- 
sion of the diagnostic indications of the feces. In the first place, it 
must be remembered that the quantity of the feces depends upon 
the quantity of the food, and again that the quantity varies with the 
character of the food, for if the food be such as to be bulky, yet con- 
tain ; little nutritive material, there will be a large residue to be 
passed out in the feces; whereas if the food be almost entirely com- 
posed of materials which can be assimilated very little residue is left, 
and the feces are consequently smaller in bulk. Thus, the cow eats 
a large bulk of food and passes large amounts of fecal matter, while 
the dog eats meat and passes very small amounts of fecal matter. 

Again, it is not to be forgotten that many foods actually increase 
intestinal peristalsis, and so produce large and loose movements, as 
oatmeal and wheaten grits or apples, while other foods, such as 
cheese, do the opposite. If the stools are large and copious and the 
food which the patient has taken is not of a kind leaving a large 
residue in the bowel, the indication is that there is non-absorp- 
tion of nutritive materials, with probable wasting of the patient. 

The consistency of the feces in health varies from a formed " stool" 
to a mushy condition; but in disease we have a liquid watery stool 
if the trouble be serous diarrhea, and a pasty or slimy stool if it be 
due to a catarrhal state of the bowels. The passage of hard scybalous 
masses mixed with liquid indicates that the feces have become dried 
and hard in the sacculations of the colon, and are passed only 
21 



322 THE BOWELS AND FECES 

when they cause so much irritation as to produce diarrhea. If the 
feces are in narrow bands or flattened ribbon-shapes, there is prob- 
ably a stricture of the rectum, offering an obstruction to their passage. 
A mushy or semi-watery stool is often seen in typhoid fever. 

The odor of the stools depends very largely upon the food which 
is taken and upon the degree of fermentation present in the bowels. 
In nursing children the stools often have a faintly sour odor, and in 
the diarrhea of nurslings with acid fermentation there is an odor of 
the fatty acids. If the process is marked, this odor becomes actually 
foul, and in cholera infantum the stools have a musty, mou y odor. 
If malignant growth of the bowel is present, the odor is fetid, as it is 
also in gangrene of the intestine. Sulphur when taken internally 
sometimes causes a very offensive stool, owing to the sulphuretted 
hydrogen gas which is developed in the bowel. 

The color of the stools is of great diagnostic importance in several 
conditions. In health the feces should be brown or brownish black, 
the color being partly due to the food, but chiefly to the bile (hydro- 
bilirubin). Certain fruits render the stools dark in color, and some 
drugs, such as iron and bismuth, make them black, and hematoxylon 
often makes them look red. 

In the stools of persons living on a pure milk diet we usually find 
little color comparatively. Again, in cases of jaundice, phosphorus 
poisoning, and acute yellow atrophy of the liver, the stools are very 
light in color, owing to their lack of biliary coloring. They are also 
apt to be very light in chronic lead poisoning. 

Bilious stools are either golden yellow, greenish, or reddish in hue, 
and if the flow of bile is profuse, they are apt to be watery. Greenish 
stools looking as if they contained chopped spinach are, however, 
a peculiarity of the diarrhea of fermentation, particularly in infants, 
the color being due to color-forming microorganisms ; but a greenish 
stool may also be produced in an infant by the persistent adminis- 
tration of sodium bicarbonate. 

If the stools are well mixed with mucus, the catarrhal process 
probably exists in the ileum; but if they consist of hard masses of 
feces coated with mucus, the disease is probably a colitis. 

Bloody stools are most commonly due to hemorrhoids which are 
eroded. The blood may be bright if the hemorrhoid be a small 
arterial bunch, or more dark and grumous if slow oozing has gone on 
for some time prior to the movement. As a rule, the brighter the 
blood in the stool the nearer its source is to the anus, and the darker 
the blood the higher is its source in the bowel. Thus, if the stools 
are tarry-looking, the blood is almost certainly from the small intes- 
tine, and probably arises from a duodenal or other ulcer or from 
carcinoma of the stomach or bowel; while if it is only somewhat 
changed in appearance, it may be due to an ulcer or ulcerated morbid 



occult BLOOD 323 

growth in the colon. Sometimes, however, when the hemorrhage 
from the ileum is very profuse, as in typhoid fever, the blood comes 
from the anus only slightly changed in appearance. 

Occult Blood. — Blood in the feces in such quantities as not to be 
recognized except by careful tests forms a very important diagnostic 
aid in cases of suspected gastric or duodenal nicer or cancer, in 
cirrhosis of the liver, and even in typhoid fever when it is feared that 
deep ulceration of the bowel will result in free hemorrhage. The 
best test for "occult blood" is the so-called aloin-turpentine test. 
Before this is used rare meat must be excluded from the patient's 
diet and the test should not be regarded as negative in its results so 
far as determining a leakage of blood is concerned until several tests 
have been made covering a period of a number of days, as oozing 
hemorrhage is often inconstant. Blood from hemorrhoids or figure 
of the anus must be excluded of course. The test as employed by 
J. Dutton Steele is as follows: 

If the stools are not in a semiliquid condition they must be made 
so by thoroughly mixing them with distilled water. 5 gin. of fecal 
matter are used in every test. After the material has been completely 
softened the feces must then be thoroughly mixed with at least its 
own bulk of ether, and the whole well shaken. 'This is a very neces- 
sary part of the procedure, as it removes the fat, which otherwise 
produces a thick emulsion when the stools are extracted with acetic 
acid and ether, and renders it almost impossible to obtain a satisfac- 
tory ethereal extract. After being thoroughly shaken the mixture 
of feces and ether should be allowed to stand for fifteen minutes or 
longer and the supernatant liquor is then poured off. The remaining 
fecal matter is then mixed with one-third its volume of glacial acetic 
acid and 10 c.c. of ether. The mixture is again shaken and allowed 
to stand for at least fifteen minutes. The ethereal extract will rise 
to the top in a clear layer and can be readily poured off. 

The solution of aloin used is made by dissolving as much aloin as 
will go on the end of a spatula in one-third of a test tube of 70 per 
cent, alcohol; 2 or 3 c.c. of the clear yellow aloin solution are then 
mixed in the test tube with about the same amount of the ethereal 
acetic acid extract; 2 or 3 c.c. of ozonized turpentine are next added 
and the whole is gently shaken. If blood is present the reaction may 
appear in one of several ways: either the whole mixture turns a 
pink which gradually deepens to a cherry red, or the solution of 
aloin sinks to the bottom and forms a layer beneath the mixture of 
ether and turpentine, and this lower layer of aloin in positive tests 
gradually becomes a deep cherry red. Sometimes if the ether and 
turpentine are first mixed and then the aloin allowed to flow gently 
down the side of the tube, the two sets of fluids will remain separate 
and a deep red ring will form at their junction. Not more than fifteen 



324 THE BOWELS AND FECES 

minutes should be allowed for the red color to show itself, for after 
this the aloin will gradually turn red, even if blood is not present. It 
is extremely important to make up the solution of aloin freshly, for 
when it stands exposed to light it changes into about the color that 
it attains in the reaction when blood is present. When the test is 
negative the color remains a light yellow, which becomes a red after 
standing for some length of time. Hydrogen peroxide does not work 
satisfactorily as a substitute for turpentine in the aloin test. 

The ozonized oil of turpentine should be prepared by allowing a 
chemically pure oil of turpentine, such as that prepared by Merck, 
to stand exposed to the air for at least three weeks. 

Stools containing pus may receive this material from the surfaces 
of ulcers, but usually the source of the purulent matter, if it is 
present in large amount, is an abscess which has ruptured into the 
bowel, as, for example, in perirectal, or even subphrenic abscess. 

Finally, we may find gallstones in the stools, which, if they are 
passed soon after their escape into the bowel, are found to be faceted. 
Stools which are being searched for gallstones should be washed 
through a sieve in such a way as to catch the stone and let the fecal 
matter through. The intrahepatic gallstone is not faceted and crum- 
bles easily. This stone rarely escapes, because it is embedded, and if 
it does get into the bowel is usually broken up. All stones or concre- 
tions found in the feces are not to be considered as gallstones. They 
may be pancreatic calculi in rare instances, or they may be fecal 
stones (coproliths) or intestinal stones (enteroliths). Fecal stones 
are simply hard inspissated masses of feces, which may attain a very 
large size, whereas intestinal stones are composed of heavy, brown 
concentric layers of phosphates of calcium and magnesium around 
some nidus, as a seed or piece of bone. Sometimes they are concre- 
tions of insoluble drugs, such as salol or magnesium carbonate. 

Intestinal sand appears to be a characteristic symptom of certain 
types of neurasthenia which is often provocative simultaneously 
of mucomembranous colitis. The chief constituent of intestinal 
sand is said to be calcium sulphate. Care must be taken to separate 
true intestinal sand from small seeds or the small sand-like bodies 
found about the seed core of pears. 

Very rarely a portion of the bowel sloughs away, and yet recovery 
takes place. This is seen sometimes in intussusception. 



INTESTINAL PARASITES. 

Aside from the character of the stools themselves, we often search 
for the cause of an ailment in the passages, either for foreign bodies, 
such as pebbles or pins, or for intestinal parasites (worms). Some- 



INTESTINAL PARASITES 



32; 



times worms may exist for long periods of time in the bowel without 
causing any symptoms, and, again, in childrenjin particular, they 




Fig. 129. — Ascaris lumbricoides dissected 
and walls thrown back. a. Genital orifice. 
b. Intestine, c. Oviducts, d. Longitudinal 
band. e. Ovaries. (Heller.) 



Fig. 130.— Oxyuris vermicularis maguified. 
a. Young female, b. Male. c. Mature female, 
full of eggs. (Payne.) 



cause great systemic disturbance by producing disorder of the diges- 
tion or reflex irritation. 



326 



THE BOWELS AND FECES 



Under the name of tape-worm or cestodes we find in the intestine, 
and often in the stools, a parasite occurring in segments which are 
flat and ribbon-like, and usually from a quarter to one-half inch in 
length. The worm itself may be several yards long. Its head is 
small, and it maintains its hold on the bowel by its head. The seg- 
ments are usually broken off one by one and escape in the stools, 
and the stools also contain the ova or eggs of the parasite, which 




Fig. 131. — Trichocephalus dispar, natural size. 
a. Female, b. Male. (Payne.) 



& 



are developed in each segment, which also pos- 
sesses male and female organs. 

According to the shape of the head and the size 
of the worm and the source of infection, we divide 
tape-worms into three classes: the Tenia solium, 
the Tenia mediocanellata, and the Bothriocephalus 
latus. 

If the patient passes a worm of from one to three 
yards in length, the head of which is about the size 
of a pin-head and glistening gray in appearance, the 
rest of the worm being yellowish white, and if upon 
the head can be seen four pigmented suckers sur- 
rounded by a crown of hooks, that worm is a Tenia 
solium, and is probably derived by the patient from 
raw or uncooked pork. The eggs of the tenia 
solium must be sought for by a microscope. They 
are round and covered by a hard shell, which 
upon pressure breaks into small fragments. In a b 

the shells may be found a few booklets. These eggs fig. 132.— Ankyiosto- 
are passed out in the feces by the host, and are then ™ auodenaie mag- 

f, ,. .. , J ill iii nified. a. Male. 6. 

swallowed by the pig, in whose muscles the booklets Female. (Bristowe.) 
migrate and form cysts. In these cysts the hooklets 
develop, and when a man eats the meat raw they enter his intestine, 
attach themselves, and from them a tape-worm is developed. 

If the worm is from four to five yards long and the segments after 
leaving the anus have motile powers, and if the head is larger than 
that of tenia solium and devoid of hooklets about the suckers on its 
head, it is probably the Tenia mediocanellata or saginata. The egg 



tNTESTINAL PARASITES 



327 



is slightly larger than that of the solium. This worm usually comes 
from eating raw beef. The Bothriocephalus lotus is the largest of all 
tape-worms,, often reaching seven to eight yards in length. It has a 
long head with two long, narrow suckers. r [ ne eggs are oval, very 
large, and the shell is light brown in color, and very easily broken. 
This parasite is not common in America, but is a very frequent cause 
of profound anemia in the persons whom it infects. Its joints are 
only rarely thrown off, so its presence is often overlooked, and this 
renders the search for the eggs very important in severe anemia with 
no ascribable cause. This worm is usually derived from fish. A 
worm which is comparatively rare is the tenia cucumerina, which has 
a head with sixty hooks. It infects dogs, cats, and sometimes children. 




Fig. 133.— Ova and embryo of Uncinaria americana: a, unicellular ovum; 6, c, d, e, ova 
showing various stages of segmentation; /, g, ova containing larval uncinarise; h, peculiarly 
shaped ovum; i, larval worm just emerged from shell; j, larva extended after emergence. 
(Stiles.) 

A round-worm, looking like an ordinary earth-worm, appears 
sometimes in the stools, and is called Ascaris lumJ)ricoides. It is 
sometimes vomited, and rarely causes trouble by crawling into and 
blocking the common biliary duct. 

Fine thread-like worms inhabiting the rectum are the Oxyuris 
vermicular is. 

A very important diagnostic find in the feces is a worm looking 
very much like the thread-worm, but somewhat larger, which inhabits 
the duodenum. It occurs as the Ankylostomum duodcnalc sometimes 
called the Uncinaria duodenale and as the Uncinaria americana or 
Necator americana. These parasites belong to the nematodes. The 



328 THE BOWELS AND FECES 

Ankylostomum duodenale is possessed of two pairs of hook-shaped 
ventral teeth and one pair of dorsal teeth projected forward. The 
male parasite is 8 to 10 mm. long, the female is from 10 to 18 mm. 
long. The Uncinaria americana has no hook teeth but a ventral 
pair of slightly developed lips and a dorsal pair of semilunar plates 
or lips. The male is 7 to 9 mm. long and the female 9 to 11 mm. 
long. The eggs are elipsoid and contains a well-developed embryo or 
are segmented. If the stools are set aside in a warm place the embryos 
can be seen to develop under the microscope if a small part is spread 
on a slide. The worms themselves are often of a red hue. A rough 
test proposed by Stiles is to place a small part of the stool on white 
blotting paper for an hour. If it is now removed and the paper is 
stained red the worm is present. The importance of finding this 
parasite lies in the fact that it produces the most profound and acute 
anemia by sucking blood from the intestinal wall, although some 
assert that the anemia is not due to loss of blood but to a poison 
formed by the parasite. The worms are usually only found after a 
vermifuge is taken, but the eggs are always present in the feces as 
unsymmetrical, thickly covered, segmented globules. 

The so-called whip-worm, or Trichocephalus dispar, is a fine 
thread-worm without any medical interest. 



CHAPTER XI. 

THE URINARY BLADDER AND THE CJRINE. 

Disorders and diseases of the urinary bladder Retention of urine -Incon- 
tinence of urine — The characteristics of normal and abnormal urine — 
The normal and abnormal contents of the urine Their significance — 
Tests for the contents of the urine. 

THE BLADDER. 

The objective symptoms of bladder difficulties arc generally local, 
unless they are very chronic, when the face may appear worn and 



8th cervical and 1st dor 
sal segment at 7th ver- 
tebra. 



Lumbar enlargement of 
cord at loth dorsal ver- 
tebra. 



End of cord at 2d lumbar 
vertebra. 



Cauda equina 




1st to Ttli cervical 
vertebra. 



1st to 12th dorsal 

vertebra. 



■ 1st to 5th lumbar 

vertebra. 



1st to 5th sacral 
l" vertebra. 



Fig. 134. — Showing the surface areas of the back corresponding approximately to the 
areas of the spinal cord supplying the trunk, limbs, and bladder. 



weary, and, if a purulent cystitis be present, septic fever may occur. 
The subjective symptoms are tenderness, tenesmus, pain (see chapters 
on Pain and on the Abdomen), and retention or incontinence of 
urine. 



330 Ttt$ URINARY BLADDER AND THE URINE 

Retention and Incontinence of Urine. — Retention and incontinence 
of urine usually depend upon causes arising outside this viscus. It 
may arise from disease or injury which destroys or temporarily 
impairs the function of the cells in the spinal cord which govern the 
contraction of the muscles involved in expelling urine from the 
bladder. These centres are situated at or about the level at which 
are given off the second, third, and fourth sacral nerves. (See Fig. 
134.) (See also page 82.) 

Paralysis of the bladder with retention may, therefore, follow 
severe injuries to the spinal cord, produced by a fall, blows, or other 
traumatisms, or be due to a myelitis which destroys such centres. 
(See chapter on the Legs and Feet, part on Paraplegia. ) The bladder 
symptoms seen in myelitis — transverse, traumatic, or otherwise — 
usually come on in the acute form within a few hours after the sensory 
and motor disturbances have been noticed by the patient, and either 
incontinence or retention, or both, may occur. 

If, however, the myelitis is not complete, the bladder may escape. 
On the other hand, if the portion of the cord which is involved 
happens to be that part governing the bladder, vesical symptoms 
may develop before the motor symptoms are clearly marked. Again, 
it is a noteworthy fact that when recovery takes place vesical con- 
trol may be regained before any marked improvement can be found 
elsewhere. Often the loss of control of the bladder is such that 
the patient cannot voluntarily expel the urine and cannot retain it, 
and it dribbles away without his knowledge. Under such circum- 
stances there is probably a myelitis involving the lower part of the 
dorsal cord and the upper and lower parts of the lumbar cord; in 
other words, all that portion in which the vesical centres are situ- 
ated. If the dribbling of urine takes place without distention of 
the bladder, the fluid passing directly from the ureters through 
the urethra, the lower part of the lumbar enlargement of the cord 
is affected, owing to paralysis of the sphincter. On the other 
hand, distention of the bladder, due to retention of urine, occurs 
when the myelitis is in the lower dorsal and upper lumbar cord, 
and is due to paralysis of the detrusor muscles, which make no 
effort to expel the urine, while the sphincter, the centres of which 
are intact, maintains a tightly closed orifice. Such cases may empty 
the bladder spasmodically at long intervals (overflow incontinence) 
— that is, sphincter paralysis from distention may ensue. In such 
a condition the bladder should be emptied by the catheter to avoid 
paralysis and vesical disease. To put the case in another way, we 
can say that the spinal centre for the control of the walls of the 
bladder is situated at a higher point in the cord than is that for 
control of the sphincter, and, therefore, retention of urine indicates 
a lesion higher up in the cord than does incontinence without reten- 



TtiE BLADDER 331 

lion. Precisely similar vesical symptoms occur in cases of spina! 
tumor producing transverse lesions of the cord (see chapter on the 
Feet and Legs, Paraplegia), or may arise from spinal apoplexy. 

The bladder symptoms of locomotor ataxia are often quite char- 
acteristic, and are to be separated from those of myelitis, spinal 
tumor, and the vesical troubles due to traumatisms of the cord. 
The disorder depends entirely upon interference with the reflexes of 
the viscus, and so presents varying symptoms which are motor and 
sensory. The patient sometimes complains of the fact that he has 
to strain for a long time before he can start a stream, which, even 
after it is started, is often jerking or interrupted; or, again, he must 
sit down and bend over in order to have the aid of his abdominal 
muscles before he can evacuate the bladder. As a result of this, 
residual urine in excess is always present, and cystitis or milder 
degrees of vesical irritability develop. In other instances the desire 
to urinate comes upon the patient so suddenly and forcibly that the 
urine is voided before he can, with his impaired gait, reach a place 
to pass it in a proper manner; on the other hand, it may be retained 
and can only be removed by a catheter. Still others find that urine 
escapes on laughing, coughing, or sneezing, owing to lack of com- 
plete control of the bladder and its sphincter; or, again, after many 
attempts to urinate, the patient gives up the effort, only to be humili- 
ated by an involuntary passage of urine immediately after his penis 
has been withdrawn into his clothes. 

These symptoms differ so materially from those present in 
myelitis as to make a diagnosis as. to their cause nearly always 
possible. 

In obscure cases of ataxia the vesical symptoms may aid the diag- 
nosis quite markedly; thus the presence of bladder symptoms would 
confirm a diagnosis of ataxia as against pseudotabes due to periph- 
eral neuritis. Again, in myelitis the presence of vesical symptoms 
points to that disease, and excludes from the diagnosis such affec- 
tions as poliomyelitis and lateral sclerosis, affections in which vesical 
paralysis rarely, if ever, occurs. Precisely similar vesical symptoms 
are sometimes seen in cases of general paralysis of the insane, but 
the delusions of grandeur or of persecution and other characteristic 
signs of this disease separate it at once from ataxia. 

Retention sometimes comes on in locomotor ataxia, in which 
disease the impulses from the bladder are not recognized, or are 
perverted, so that the sphincter which closes the bladder does not 
relax to permit the escape of urine, or the cord or brain fails to recog- 
nize that the bladder is full, and so sends no impulse for its relief. 
Again, retention of urine may arise from paralysis of the muscular 
part of the vesical walls by pressure produced in severe labor (child- 
birth). Finally, we see cases in which the bladder cannot be 



332 THE URINARY BLADDER AND THE URINE 

emptied, because its walls have been paralyzed by overdistention 
with urine. 

Incontinence results from loss of power in the sphincter, due to 
injury or disease in the cord at the level of the second, third, and 
fourth sacral nerves; and this, by the way, is a far more frequent 
occurrence than is absolute retention. The real condition under 
these circumstances is that the expelling muscles and retention 
muscles are both paralyzed, so that the urine accumulates in 
the bladder and then dribbles through the unguarded neck of the 
bladder. Sometimes, too, this incontinence is caused by the 
urethra being so insensitive that it fails to recognize the presence 
of the urine, and so does not send an impulse to the sphincter to 
tighten its hold. Incontinence also results from excessive reflex 
irritability of the walls of the bladder, so that the urine no sooner 
trickles into this viscus than an impulse is sent to the spinal centres 
which send a motor impulse to the muscles of expulsion. This is 
often the condition in the nocturnal incontinence of children, for as 
soon as the child sleeps its will-power over the bladder ceases, and 
reflex activity is alone in control. Irritating, concentrated urine 
may pervert the reflexes of the bladder and so cause incontinence. 

Sensory Disorders. — The sensory disturbances of the bladder will 
be found discussed in the chapter on Pain, but it is worth noting 
here that accompanying the symptoms already named as charac- 
teristic of locomotor ataxia vesical crises of spasm and pain fre- 
quently occur. 

When there is pain in the bladder, made worse by the attempted 
act of micturition, and tenesmus, with pain darting into the urethra, 
there is probably present a cystitis; but the physician should remem- 
ber that cystitis may be present with almost no painful manifesta- 
tions, even when in its acute form. In other cases this condition 
arises from concentration of urine, which produces irritation of the 
viscus. In children this concentration of the urine is the most 
common cause of nocturnal urinary incontinence. 

Involuntary passage of the urine sometimes occurs in idiots, in 
some cases of insanity, in attacks of apoplexy, or any condition of 
abnormal unconsciousness, and sometimes in very severe infectious 
diseases, such, for example, as diphtheria. Oftentimes it results in 
children from irritation of the foreskin or vagina, or from rectal 
irritation produced by seat-worms, since all these causes disturb the 
reflex activity of the spinal centres. 

Obstruction to Urinary Flow. — Interference with the passage of 
urine may also arise from two causes which are surgical in char- 
acter, namely, stone in the bladder and tumors of the bladder, 
which are often situated near its neck and so produce obstruc- 
tion. Finally, in old men, that most commonly met with cause of 



THE URINE WWW 

difficult micturition, enlargement of the prostate, is to be remem- 
bered. 

Aside from these causes of interference with the passage of urine, 
we must not forget the possibility of its obstruction by stricture of 
the urethra, nor should the physician ignore the fact that some per- 
sons have "nervous bladders," which will not respond to an effort 
of the will if another person is near by, although the urine is instantly 
passed as soon as the patient is alone. 



THE URINE. 

Changes from the normal in the urine, as already stated, are 
determined, first, by its general appearance, quantity, odor, specific 
gravity; second, by its microscopic appearance; and, third, by its 
chemical reaction and responses to tests. Any changes in this fluid 
of an abnormal character are solely symptomatic, and point with 
more or less distinctness to disorders of bodily metabolism, disease 
or disorder of the kidneys, ureters, bladder, or urethra, and some- 
times of the prostate, testicles, vagina, or uterus. 

The urinary secretion is one which is too frequently ignored by 
the student and physician in studying the diagnosis of disease. In 
many instances it will, if properly tested, give such positive evidence 
in regard to obscure affections that a correct diagnosis is at once 
possible 4 , and in other cases its examination, as a matter of routine, 
will discover important facts, the existence of which has been unsus- 
pected. Again and again will a diagnosis prove erroneous if the 
importance of urinary examinations is ignored, and costly errors for 
the patient and the reputation of the physician ensue. 

In asking questions about the character of the urine passed and 
its quantity, the physician should be sure that the patient clearly 
understands his question. Often he is told that much urine is 
passed, when, in reality, it is really in small amount, but passed 
often; or that it is blood red, when red because of the presence 
of high-colored urates and uric acid. In inquiring about its color, 
we should remember that if large amounts of liquid have been 
swallowed it will probably be light in hue, or if small amounts 
of drink are taken, dark in hue. So, too, active exercise in warm 
weather may produce a somewhat concentrated urine, because 
much liquid has been lost by the skin in sweat, and the muscular 
exertion produces large quantities of nitrogenous material indicative 
of tissue waste. In winter the urinary flow is more apt to be free, 
because the skin is inactive. 

The urine which is to be tested should always be passed directly 
into the vessel in which it is brought to the physician, and this bottle 



334 THE URINARY BLADDER AND THE URINE 

should be scrupulously clean ; or, if the urine is passed into any other 
vessel, care must be taken that it is perfectly clean. When it is 
thought that urethral disease may obscure the investigation a catheter 
should be passed, all urine in the bladder drawn off, and then the 
catheter allowed to remain in place, so that the urine will trickle 
directly from the ureters to the catheter, and so to a receiving vessel. 
This is very important when the urine is voided involuntarily. If 
the condition of the bladder is bad, this viscus should be washed 
out by boric-acid injections, in order to prevent it from contami- 
nating the urine which is to be tested. 

Quantity of Urine.— The quantity of urine passed by a healthy 
adult varies from two to four pints in the twenty-four hours, 
according to the amount of liquid ingested, the freedom of per- 
spiration, and the amount of exercise. 

The significance of any great and constant increase in the amount 
of urine passed in a given case is various. Thus, we find it greatly 
increased in diabetes mellitus, in diabetes insipidus, in some cases 
of neurasthenia, and in some cases of hysteria. It is also increased 
in many cerebral lesions. Hypertrophy of the heart, particularly 
if associated with chronic contracted kidney, causes an increase in 
the urine; and, therefore, if a patient has to urinate frequently or 
has to arise at night to empty the bladder, we suspect this trouble 
if diabetes and cystitis are excluded. 

A copious flow of urine of a low specific gravity and of a pale, 
clear appearance, containing fatty, hyaline, and finely granular casts, 
is often seen in cases of amyloid disease of the kidney, and the pres- 
ence of syphilis, of prolonged suppuration, or extensive bone disease, 
due, it may be, to tuberculosis, with concomitant enlargement of 
the liver and spleen, separates it from any other ailment. Albu- 
minuria may be a marked symptom or be entirely absent. 

Polyuria also ensues if the heart and kidneys are stimulated to 
increased effort by the action of drugs, such as digitalis, caffeine, or 
alcohol. We also find an increase in urinary secretion, without its 
possessing any grave significance, in convalescence from such diseases 
as typhoid fever and pneumonia. 

The quantity of the urine is diminished in cases in which the 
heart fails to do its proper amount of work, with resulting stasis of 
the blood in the kidneys, and whenever any large amount of liquid 
is taken away from the body, as in diarrhea. It is also decreased 
by fevers and by the sweats following febrile movement. Per- 
sistent vomiting also has a similar effect. Parenchymatous nephritis, 
both acute and chronic, greatly diminishes the urine, and in grave, 
fatal illnesses urinary suppression may occur. 

The Odor. — The odor of freshly passed urine is faint, but char- 
acteristic. What is often called a "urine odor" is really due to the 



THE URINE 335 

development of ammonia in urine which lias decomposed. The 
odor is altered by many drugs and foods, notably by copaiba, 
turpentine, eucalyptus, valerian, musk, asafetida, and by asparagus. 
Diabetic urine possesses a heavy, sweet odor. 

The Color. — The naked-eye examination of the urine often gives 
very important information, if its clearness, opacity, and color are 
observed. Its clearness and color are modified by the presence of 
pigments derived from outside sources, such as the educts of carbolic- 
acid or salicylic acid, of senna or hematoxylon, and from urobilin, 
and many other substances coming from inside sources, such as 
blood and bile. Many of these causes may render it opaque, but 
there are two conditions, above all others, which make the urine 
cloudy even when freshly passed, namely, cystitis with phosphaturia 
and chyluria. After urine has stood for some hours it often becomes 
opaque, because it has undergone decomposition changes. 

When urine is dark red in color and somewhat opaque the discol- 
oration may be due to blood, hemoglobin, santonin, rhubarb, senna, 
logwood, or the presence of an excess of urates. Again, it may 
be rendered almost black, instead of red, by an excess of biliary 
coloring matter. 

A black urine is sometimes seen in cases of melanotic sarcoma, 
ochronosis, and alkaptonuria, or it may turn black after the brownish 
urine produced by carbolic acid or uva ursi has been exposed to 
the air. 

Hematuria. — If the color be due to blood or hematuria, the urine 
will be of a more or less bright red, according to the freshness of 
the sample brought to the physician and the seal of the hemor- 
rhage. If the urine has been voided several hours, it will be of 
a dingy red or smoky hue, and on standing will deposit a coffee- 
ground or reddish sediment of a somewhat flocculent appearance. 
If, on the other hand, the urine is seen as soon as passed, it may be 
a bright red or a dingy red, according to the seat of the hemor- 
rhage and the time which has elapsed since the bleeding began; if 
it has arisen in the kidney or ureter or bladder, and has been 
gradual, the mixture of blood and urine will be so intimate that 
changes in the blood will have taken place, whereas if the hemor- 
rhage has occurred, simultaneously with urination, from the neck 
of the bladder or the urethra, the blood will be almost unchanged 
when it escapes from the urethra. The presence of clots in recently 
passed urine indicates a not very recent hemorrhage, and yet one 
of such size that the urine could not by dilution completely prevent 
clotting. 

When the blood comes from the kidney some of the possible causes 
are acute parenchymatous nephritis, resulting from any one of the 
severe infectious diseases, such as scarlet fever or malarial fever; 



336 THE URINARY BLADDER AND THE URINE 

embolism, resulting from ulcerative or other forms of endocarditis, 
producing renal infarction, sepsis of the kidney, the ingestion of 
irritating drugs, such as cantharides or turpentine; and injuries of 
the back, producing rupture or other disorganization of the kidney. 
All these conditions produce what may be called acute hematuria. 
If the cause be acute nephritis from the presence of an infectious 
malady, such as scarlet fever, pain in the loins, the presence of 
albumin in the urine, and the eruption will render the diagnosis easy. 

Hematuria due to malarial poisoning may appear with the first 
malarial paroxysm, of the intermittent type, which the patient has 
ever had, and at a time when the history of the case renders it certain 
that an old malarial condition could not have previously damaged 
the renal tissues or those of other organs in the body. In other 
words, there are cases in which a free hemorrhage from the kidney 
takes place, by reason of the chill, in much the same manner in which 
hemorrhage takes place in acute nephritis due to exposure to cold 
or to irritants. Under these circumstances there may or may not be 
developed a true organic lesion of the kidney in the sense of per- 
manent disease. 

Secondly, we have cases in which bloody urine appears, not in the 
first malarial paroxysm of the intermittent type, but in association 
with the later attacks, which may have followed the first either rapidly 
or slowly. In these cases there may be no further cause for the 
hemorrhage than excessive congestion, but in all probability the 
vast majority of such patients present distinct renal changes, which 
permit such a symptom to develop when the paroxysm asserts itself. 

Thirdly, we pass from those cases of bloody urine due to inter- 
mittent forms to those due to remittent attack. In these patients 
the process by which a bloody colored urine is developed may be 
very complicated, since it may be due to renal disease, functional or 
organic, or to a true hemoglobinuria, arising from dissolution of 
the red blood cells in the bloodvessels or blood-making organs. 

Finally, there is a type of malarial hematuria which is brought 
on by the administration of quinine (Karamitsas and others). 

All these forms of hematuria can be diagnosticated by the presence 
of the malarial parasite in the blood (see Chapter on the Blood) and 
the characteristic malarial symptoms, except that which occurs in 
persons who have a dyscrasia from old malarial poisoning when 
no organisms are found. 

If the hematuria be due to embolic infarction of the kidney, an 
examination of the heart will probably reveal signs of valvular 
disease, from which source the embolus will have resulted, or in 
other cases the physical signs, combined with the history, will show 
malignant endocarditis with renal sepsis therefrom. Sometimes 
thrombosis of a renal vein occurs in feeble, wasted infants, and so 



THE URINE :y.>u 

causes hematuria. If embolism is not the cause of tli<- hematuria, 
the history of the ingestion of an irritating drug will be the diag- 
nostic guide, or, if injuries be the cause, a history of trauma will 
elucidate the case. 

The causes of chronic or persistent hemorrhage from the kidney 
are chronic diffuse nephritis, cancer of the kidney, calculus in the 
pelvis of the kidney producing ulceration, injury of the kidney by 
jarring of a stone, tuberculosis of the kidney, and cystic degeneration. 
It is often an early symptom of hypernephroma. 

If the chronic hematuria arise from chronic diffuse nephritis, 
which is rarely the case, the diagnosis may be aided by pallor of 
the skin, anorexia, nausea, headache, decreased amount of urine, 
and albuminuria. The cause of the nephritis and the source of the 
bleeding demands careful investigation in such cases. It has been 
pointed out by Chute and others that it is quite possible for an acute 
infection to involve only one kidney or only part of one kidney, 
whereas a toxic nephritis due to a systemic poison naturally involves 
both kidneys. The history of the case and the use of the cyto- 
scope, or the ureteral catheter, will determine whether the blood 
comes from one kidney, and if this be the case and the bleeding is 
excessive a nephrectomy may be needful to save life. On the other 
hand, if the history is one which indicates a toxic nephritis in which 
state both the kidneys are probably affected and if it is found that 
the blood comes from both kidneys then nephrectomy is contra-indi- 
cated, since the remaining kidney would be unable to maintain life 
and the hemorrhage would not be arrested. A bacteriological 
examination of the urine from one ureter which reveals infection, 
while the urine from the other ureter is sterile may also aid the 
diagnosis. 

If the cause be renal cancer, the cachexia, pain, and the mixture 
of pus, blood, and disorganized renal tissue in the urine will render 
the diagnosis possible. If due to calculus, there may be a previous 
history of attacks of renal colic or of violent pain in the kidney; 
and if ulceration of the renal pelvis has occurred, there will be dis- 
turbances of the body temperature, pain in the lumbar area, and 
pus in the urine. The presence of tubercle bacilli in the urine 
decides the presence of renal tuberculosis. If cystic degeneration is 
present, it can only be determined when the cyst is large enough to 
be felt. A sudden profuse hemorrhage in the urine, sufficiently 
large to endanger life, may come from such a cystic tumor of the 
kidney. 

Blood from the kidney usually possesses the following character- 
istics: it is well mixed with the urine, and is generally altered in 
appearance, to the naked eye and under the microscope, both as to 
color and the shape of the corpuscles which may appear as the pale, 
22 



338 THE URINARY BLADDER AND THE URINE 

almost invisible bodies known as "shadow corpuscles." The cells 
and casts which may be present are changed in color by the hemo- 
globin which is free in the urine. Again, blood casts or red blood 
corpuscles clinging to casts indicate renal hemorrhage. When the 
blood comes from the pelvis of the kidney it may appear in the urine 
in long, worm-like clots (moulds of the ureter), and their extrusion 
from the ureter produces symptoms of colic. Under such circum- 
stances there may be alternations of hematuria and normal urine, 
due to the blocking of the ureter on the diseased side by a clot, 
so that all the voided urine comes from the healthy kidney. 

Blood in the urine may arise from the bladder walls and be due 
to an acute cystitis, to papilloma, malignant growth, or tuberculosis 
of this viscus, or to injury. These vesical causes should, if possible, 
be determined by the use of the cystoscope. 

It must not be forgotten also that blood in the urine may be due 
to menstrual discharge, to blood from uterine fibroids or malignant 
uterine ulceration, and that it is possible for a malingerer to place 
blood in the urine, with the object of deception. Rarely in certain 
cases of locomotor ataxia, hematuria develops after the vesical crises 
which have already been described (see Bladder in this chapter). 
This is due to capillary hemorrhage from the bladder walls. 




Fig. 135. — Distoma hematobium, male and female. The two small bodies are the eggs. 

There are other varieties of hematuria which must not be for- 
gotten, although comparatively rare, namely, that due to the presence 
in the blood of the Filaria sanguinis hominis, which is a condition in 
which the presence of chyle in the urine so masks that of the blood 
that the urine has the appearance of pinkish cream or milk, but 
microscopic examination will show blood corpuscles and fat globules, 
as well as the embryos of the filaria. (See Chyluria in this chapter.) 
Another still more rare cause of hematuria is the Distoma hema- 
tobium of Egypt and Abyssinia (Fig. 135). This produces what 
has been called tropical hematuria. The third cause is even more 
rare in man, namely, the Strongylus gigas, which also causes pyelitis 
and renal colic. A fourth form of hematuria is that seen in some 
cases of scurvy, particularly of the infantile type, and, lastly, hema- 
turia may also appear as a symptom of purpura hemorrhagica, 
hemophilia, and very rarely in leukemia. 

Hemoglobinuria. — The urine, when not discolored by blood, may 
be discolored by the presence of the coloring matter of the blood, 
This is called hemoglobinuria. 



THE I RINE 



339 



The following table, based on Purdy's well-known work on 
Urinary Analysis, sums up these conditions and their significance: 



Milkv. 



; <»R. 


Causi nation. 


Tat:: 


Nearly eoloi 


Dilution, or diminution 
of normal pigments. 


Nervous conditions : 
hydruria, diabetes insipidus, 
contracted kidnfey. 



Dark yellow to Increase of normal, or occur- Acute infectious dis 

brown red. rence «»t' pathological, 

pigm< nt-. 



Fat-globules. 



Chvluria. 





Pus-corpus 


Suppuratn of the. 
urinary tract. 


Orange. 


Excreted drugs. 


Santonin, chrysophanic acid, 
>i una. 


Red or reddish. 


Unchanged haemoglobin. 


H;eliloirl 

or hemoglobinuria. 


Pigments in food dogwood, 
madder, bilberries, fuchsin). 







llainatin. 


Small hemorrhages. 


Brown to 


Ifethsemoglobin. 


Mctlnemoglobinuria. 


brown black. 


Melanin. 


Melanotic sarcoma. 




Hydrochinon and catechin. 


Carbolic-acid poisoning. 


Greenish yellow. 
greenish brown, ap- 


Bile-pigments. 


Jaundice. 



preaching black. 



Dirty green 
or blue. 



A dark -blue scum on sur- Cholera, typhus: seen es- 
face. with a blue deposit, due pecially when the urine is 
to an excess of indigo-forming putrefying, 
substances. Indol. Methylene 
blue. 



Brown yellow to Substances which areintro- 

red brown, beconi- duced into the system with 

ing blood red upon senna, rhubarb, and cheli- 

adding alkalies. donium. 



340 THE URINARY BLADDER AND THE URINE 

Hemoglobinuria arises from a number of causes, such as infectious 
disease, poisoning by mushrooms, and excessive doses of certain coal- 
tar derivatives, or of chlorate of potassium, or glycerin. Malarial 
poisoning sometimes causes it instead of hematuria. One form 
of malarial hemoglobinuria is intermittent, the urine being at one 
hour limpid, the next hour bloody, and the third hour again clear. 

The possibility of confusing the hemoglobinuria of idiosyncrasy, 
when in a severe form, with that due to severe malarial poisoning, is 
very great, for the history of paroxysmal hemoglobinuria teems with 
reports of cases in which the chief manifestations of a malarial attack 
were present, such as chills, fever, and sweats. Probably many 
cases of so-called malarial hemoglobinuria are due to another 
parasite not as yet isolated. Hemoglobinuria also follows severe 
burns and the transfusion of human blood, and occurs in paroxys- 
mal hemoglobinuria, a condition which seems to be produced by 
mere chilling of the surface of the body or even by immersing the 
hands of a susceptible person in iced water. It may also be produced 
either by exposure to cold and damp or to the chill of the milder 
forms of malarial paroxysm. Hemoglobinuria may also be a symp- 
tom of that curious vasomotor affection called Raynaud's disease. 

Microscopic examination of the urine in such cases will show 
no corpuscles, although the urine will be coagulated by the nitric- 
acid test; but the coagulum does not settle in flakes, as it usually 
does in albuminous urine, but floats on the surface in a brownish 
mass. The naked-eye appearance of the urine is that of clear port 
wine. If a few drops of this urine be placed on a watch-glass and 
a drop of strong acetic acid be added, the blood crystals of Teich- 
mann will be found by the aid of the microscope, snowing that the 
coloring matter is hemoglobin. 

If the discoloration of the urine be due to blood rather than to 
hemoglobin, a microscopic examination will reveal red blood corpus- 
cles, white blood corpuscles, and perhaps fine filaments of clots; 
but the corpuscles will not be found in rouleaux, as in ordinary 
blood outside the body, and they may be crenated and distorted in 
shape, particularly if the urine is alkaline. (For clinical tests, see 
later text.) 

Dark Urine not Due to Blood. — If the urine be red from other 
causes than blood, this may be due to the ingestion of logwood. 
The history of the ingestion of this substance will clear up the 
diagnosis. If it be due to senna, it will be carmine, due to the 
chrysophan in this drug; but this discoloration only appears if the 
urine is alkaline. Precisely similar changes are due to the taking 
of rhubarb. So in santonin poisoning a blood-red urine is some- 
times seen, but it usually attains this appearance after being at 
first yellow, then saffron, and then purple red. One of the condi- 



THE URINE 341 

tions of the urine, due to a poison, which can be readily confused 
with hemoglobinuria or hematuria, is that produced by carbolic 
acid. This color is not due to blood, but to oxidized educts of the 
acid. The same educts produce a similar discoloration after 
naphthalin, creosote, and uva ursi have been taken in overdo-c 

Red urine, due to none of the causes which have been enumerated, 
may be due to an excess of urates (except urate of sodium, which is 
usually white). If on the addition of nitric acid the urine become- 
brown where the fluids join, the coloration is due to urates; but if 
all the fluid is browm, the patient has probably been taking freely 
iodine or compounds of iodine. 

Finally, the urine is often dark reddish brown or porter colored 
in jaundice, owing to the presence in it of biliary coloring matter-. 
Under these circumstances it may be clear or opaque, and the fluid 
is apt to be frothy on shaking and to have a decreased surface tension, 
so that powdered sulphur rapidly sinks to the bottom of the vessel, 
when the sulphur is dropped on the urine. These biliary colors are 
at once recognized by the reaction with nitric acid in Gmelin's 
test, for if a little of the urine be placed on a white plate and nitric 
acid be allowed to touch the margin of the wet place, a play of colors 
from green to blue, blue to violet, and violet to red occurs. The 
same test can be used by wetting bibulous paper with urine, and the 
acid, if brought to the edge, will stain the paper in the colors named. 
Green is the only characteristic of the biliary reaction, for indican 
gives with nitric acid the other colors. (For the symptoms of jaun- 
dice, see chapter on the Skin.) 

A greenish-colored urine is seen in cases of poisoning by salicylic 
acid, due to the indican and pyrocatechin, and after the use of 
saffron. Not rarely a greenish or blue urine is due to the ingestion 
of methylene blue, either as a medicine, as in the treatment of 
gonorrhea, or in candies colored by this dye. 

Indicanuria is present in intestinal obstruction, intestinal putrefac- 
tion, cholera, cancer of the liver or stomach, and pernicious anemia. 
It may, however, be present in health as a result of constipation. 
(See Chemical Tests.) When through disease processes indican is 
formed and excreted in the urine, it may by oxidation be trans- 
formed into a blue color (indigotin) or into a red hue (indirubin). 
If urine containing indican be treated with two or three times its 
volume of hydrochloric acid, it will turn a violet hue. 

White or Milky-looking Urine is seen in that condition called 
chyluria, due to the presence of the filaria sanguinis hominis in the 
blood. This urine on standing forms a creamy layer on its surface, 
and, if it is shaken with ether, some of the fat can be removed, 
rendering the urine clear. The diagnosis can only be confused by 
urine becoming mixed with milk or cream, and can always be made 



342 THE URINARY BLADDER AND THE URINE 

if the embryos of the fllaria be found in the urine. They lie in very 
delicate sheaths, and show a constant vibratory movement. The 
•diagnosis is still further confirmed if filaria are found in the blood, 
where they are present in large numbers at night. (See chapter 
on the Blood.) 

Urine may have a somewhat milky white appearance from an 
excess of phosphates, mixed with more or less mucus, as in catarrh 
of the bladder. A similar appearance may be due to the presence 
of pus. 

Pus. — Should much pus be present in the urine, it is probably 
derived from a pyelitis or a suppurative inflammation of the pelvis 
of the kidney. The symptoms of this state are, briefly, a constant 
or intermittent pyuria, usually an acid reaction of the urine, chills and 
fever, which may mislead the physician into a diagnosis of malarial 
poisoning, or, in other cases, if the pyelitis be tuberculous, hectic 
fever may be present. Sometimes violent attacks of pain resembling 
renal colic occur, and not uncommonly anemia and loss of strength 
are notable. There is often pain in the back, which is made worse 
by pressure with the hand, and, rarely, if the suppurative process 
be marked, typhoid symptoms may be present. 

If tuberculosis of the kidney is present, tubercle bacilli may be 
found in the urine in addition to pus and blood. The blood at 
times may be present in large quantities. The use of a segregator, 
or ureteral catheter, or the cystoscope may show nearly pure pus 
flowing from one ureter. The discovery of tuberculosis of the 
kidney is of the greatest importance because it is unilateral in 90 
per cent, of the cases according to Be van and usually primary so 
far as the rest of the genito-urinary tract is concerned. The removal 
of such a kidney, before the general health is greatly impaired, may 
save the patient's life. 

If pyuria is due to a calculus, there may be a history of gravel 
and renal colic. The purulent urine of pyelitis is to be separated 
from that of cystitis by the fact that in the former the urine is acid, 
in cystitis it is ammoniacal. Additional aids to the diagnosis are 
the pain in the renal region, often unilateral; and the use of the 
cystoscope to exclude vesical disease. The prognosis varies. If 
due to an infectious fever, recovery usually occurs. 

Specific Gravity. — After having examined the urine with the naked 
eye and by suitable tests, the physician proceeds to study it by the 
aid of the urinometer or specific gravity apparatus. This consists 
of a tall, straight glass into which the urine is poured at the tem- 
perature of 60° F. The specific gravity flask is now gently lowered 
into this fluid and allowed to float in it freely, the container being 
exactly filled, care being taken that no bubbles of air adhere to the 
bulb or to the upper end of the flask, since these will float it and help 



THE URINE 343 

to raise it out of the urine, thereby giving a fictitious reading of the 
scale on its stem. The urine used in the urinometer should be, if 
possible, a sample from the total amount passed in twenty-four 
hours, since the specific gravity of this secretion varies at different 
times of the day, and a single specimen may give an incorrect idea 
of the real specific gravity of the total amount of the fluid. When 
the physician is desirous of determining the total amount of solids 
excreted in twenty-four hours from the specific gravity the precau- 
tion of taking the specific gravity of the total quantity of urine is 
particularly important (see below). The normal specific gravity 
varies from 1015 to 102."). 

The specific gravity of abnormal urine varies from 1005 to 1040 at 
60° F.; but a persistently low specific gravity indicates chronic con- 
tracted kidney if no dietetic cause can be found, while a persistently 
high specific gravity either shows concentration of the urine as the 
result of fever or parenchymatous nephritis, or, if the urine is very 
light in color, the cause is perhaps diabetes mellitus, the high specific 
gravity being due to the sugar which it contains. 

The Total Quantity of Solids excreted by the kidneys in twenty- 
four hours can be roughly estimated by taking the specific gravity 
of the total quantity of urine passed during that time, and then 
multiplying the last two figures of this specific gravity by 2. The 
number obtained represents the total amount of solids in 1000 c.c. 
of urine. Thus, supposing the urine to have a specific gravity of 
102,"), we would find that 25x2 = 50 gm. Instead of this means, we 
can also resort to what is known as Haine's modification of Haser's 
method, although if the solids are much decreased, more accurate 
methods of testing should be resorted to. The method just referred 
to is carried out as follows: the last two figures of the specific gravity 
of the urine are multiplied by the number of ounces voided in twenty- 
four hours, and the product is multiplied by 1.1. Thus, if a patient 
passes 32 ounces, and the specific gravity of the urine is 1012, we 
multiply 32 by 12, which equals 384, and this is multiplied by 1.1, 
which equals 422, which would be much less than the normal for 
a person of, say, 150 pounds, who should pass about 945 grains of 
solids in twenty-four hours. 

This estimation of the total quantity of solids eliminated in the 
twenty-four hours is of great diagnostic and therapeutic value. It 
has been found as the result of an immense amount of research 
that a healthy person of about 145 pounds' weight, and from twenty 
to thirty years of age, taking an ordinary diet and ordinary exercise, 
should eliminate 61.14 grams or 945 grains of solids in twenty-four 
hours. In the patient between forty and fifty years of age, we must 
deduct 10 per cent, from this. If between fifty and sixty, 20 per 
cent.; if between sixty and seventy, 30 per cent. In patients over 



344 THE URINARY BLADDER AND THE URINE 

seventy, 50 per cent. If a patient is on a very light diet, we must 
deduct 15 per cent, from the average solids, and if at rest and free 
from exercise, 10 per cent. If it be found that a patient is persist- 
ently eliminating much less solids than normal, we should consider 
that he has renal inactivity, and it is our duty to give diuretics. 
This is particularly the case in fevers, in which there is great tissue 
waste, so that the solids ought to be greatly increased above the 
normal. If they are not eliminated, danger is present from their 
retention. (For accurate estimation of urea, see Chemical Tests). 

As a further guide to determine the activity of the kidney, we may 
employ the so-called methylene-blue test, which consists in injecting 
into one of the muscles of the thigh 1 grain of methylene blue in 10 
minims of water. Ordinarily the blue appears in the urine within 
half an hour, and disappears within thirty-six to forty-eight hours; 
whereas in disease of the kidney, its primary appearance is delayed, 
and it remains present for several days because the kidney is not 
competent speedily to eliminate it from the system. 

In chronic contracted kidney the color may be present in the urine 
after fifteen days. 

If too large a dose is given the color may appear very quickly even 
in cases of disease. 

This is not a positive test, because one part of the kidney 
concerned with the elimination of one substance may be diseased 
while another is in health. The rapidity with which absorption 
takes place from the tissues must also be considered. This is seriously 
impaired in anasarca and when the circulation is very feeble. 



MICROSCOPIC APPEARANCE OF THE URINE AND 
ITS CONTENTS. 

Having considered the macroscopic appearance of the urine, we 
may turn to its microscopic appearance, and this part of the subject 
is of even greater importance than the study of the gross appear- 
ance of this secretion, for, very commonly, a sample of urine which 
looks quite normal to the naked eye is loaded with microscopic 
objects of the greatest pathological significance. The most impor- 
tant of these objects are what are called "casts" — that is, moulds of 
the uriniferous tubules, formed as a result of the disease process 
present in the kidney. These casts consist of epithelial cells, blood 
corpuscles, and pus corpuscles, masses of microorganisms, or of 
broken-down organic matter, as in fatty casts, and in hyaline or 
transparent bodies, or moulds which are made up of unknown 
material, but often covered by corpuscles, pus corpuscles, or epi- 
thelial cells In addition to these bodies we find a large number of 



MICROSCOPIC APPEARANCE OF URINE AND ITS CONTENTS 3 \r, 

organic bodies or derivatives of organic matter, and inorganic sub- 
stances derived from the tissues or from food. 

The physician who desires to examine urine successfully by the aid 
of the microscope must bear in mind that it can be examined satis- 
factorily after it has stood still in a glass or other vessel for a long 
enough time to allow sedimentation to take place — that is, until the 
objects floating in the fluid have had time to settle, or employ a 
more rapid method of obtaining the sediment by the use of the cen- 
trifuge, an apparatus by means of which the solids in a fluid arc 
separated by centrifugal force. By the use of this apparatus a sedi- 
ment can be obtained in a few minutes after the urine is passed. 
(See Fig. 136, and for a description of the principle of the apparatus, 
see chapter on the Blood.) 

The sediment is to be drawn up into a pipette which has been 
introduced into the urine and a drop placed upon a glass slide, 
covered by a cover-glass and the slide placed under the microscope. 




Fig. 136. — Holder for urine tube in centrifuge. 



Casts composed of epithelial cells present an appearance similar 
to that seen in Fig. 137, and are due to proliferation or exfoliation 
of the epithelium lining the uriniferous tubules. The cells look 
swollen and granular and may contain globules of fat. These 
epithelial casts occur in three forms: first, they may appear as hollow 
casts of the tubule when the epithelium has exfoliated en masse {that 
is, the lining of the tube is cast off in one piece); second, they appear 
as casts made up of epithelial cells glued to one another; and, third, 
the cells are attached to the surface of a clear, transparent basis, 
looking like a hyaline cast. All these varieties are highly refractive 
of light and are not altered by chemical substances as easily as are 
the other casts about to be described. 

Having found bodies of this sort in the urinary sediment, what 
is their significance? At one time they were considered a positive 
sign of an inflammatory process in the parenchyma of the kidney, 
or, in other words, of parenchymatous nephritis, but at present we 



34G 



THE URINARY BLADDER AND THE URINE 



know that almost every sample of urine if centrifuged for some 
minutes will yield a few hyaline casts. 

Blood casts consist of more or less well-preserved blood corpuscles 
attached to one another in a mould of the tube in which they have 
escaped. They are rarely seen and are masked by freely floating 
cells. The significance of these blood casts is great, as they indicate 
an acute inflammation of the kidney, acute congestion of this organ, 
or a renal infarction. They are of importance, too, in separating 
hematuria arising from other sources than the kidney from hemor- 
rhage from this organ, because they are not found unless the escape 
of blood has been into the uriniferous tubules. 

Casts composed of pus corpuscles are still more rarely seen, but, 
if constantly present, may indicate multiple abscess of the kidneys. 




Fig. 137. — Casts containing epithelial cells. (Peyer.) 

When masses of micrococci become grouped together in the 
tubules they may be expelled in casts, and under a low power look 
somewhat like granular casts (see below). They can be seen to 
consist of micrococci if a higher power is used, and they are not 
quickly changed by acids, as are casts composed of other materials. 

The significance of their discovery is that septic infection of the 
kidney is present, as the result, it may be, of septic embolus brought 
from a distant infected part. They are seen in suppurative renal 
inflammation and in cases of pyelonephritis in which the true renal 
tissues are being involved by an extension of the disease. 

Casts, composed of broken-down organic matter, are found as 
granular and fatty bodies; that is, they represent broken-down 
blood corpuscles and epithelial cells, and their appearance varies 



PLATE X. 



Fig. 1. 



Fig. 2. 



3^5 

O o o o ° o c 

O ° o c ° ° • 

O _ 0°o 





Fatty, Waxy, Hyaline, and Granular Casts. 



Uric Acid Crystals. 



Fig. 3. 



Fig. 4. 



k 6 v 








Ammonium Urate Crystals. 



Epithelial Cells. 

A, squamous epithelium ; B. bladder epithelium ; 
C, kidney epithelium ; D. kidney epithelium (fatty). 



MICROSCOPIC APPEARANCE OF URINE AND ITS CONTENTS 347 

greatly according to the stage of the process and the origin of the 
materials composing them. Thus, the granular appearance may be 
very fine, as shown in Fig. 138, or light and refractive, dark or 
opaque. Very often the edges of these casts are irregular and the 
ends frayed and uneven. The color of these bodies may be yellow, 
brown, or grayish. 

The significance of granular casts is grave. They are usually 
present in large numbers in chronic parenchymatous nephritis. If 
they are not very granular and are only found in small numbers in 
centrifuged urine they possess less importance. 

Fatty casts, composed of minute globules of oil, cohering to one 
another or attached to a central core of epithelium, or fat crystals, 




Fig. 138. 



-a, a. Epithelial casts, b, b. Opaque granular casts from a case of acute 
Bright's disease. ( Roberts. ) 



are found in cases of widespread fatty degeneration, as the result of 
disease or poisoning, as in the case of large white kidney, on the one 
hand, or phosphoru , arsenical, antimonial, or iodoform poisoning, 
on the other. They show the presence of a very slow process if due 
to disease, but have not the same significance if caused bv poison. 
(See Plate X, Fig. 1.) 

Hyaline casts are long, worm-like, transparent bodies, sometimes 
with very fine granulation, particularly along the edges, and because 
they are transparent they are often hard to find. These bodies 
are supposed to be composed of albumin which has been exuded 
into the tubules. They may be found in the urine in any type of 
nephritis or even when nephritis is not present, but when they are 
the only cast found and the urine possesses certain other characters, 



348 



THE URINARY BLADDER AND THE URINE 



their significance is exceedingly grave, particularly if they are present 
in great numbers, as they point very strongly to that incurable 
malady, chronic interstitial nephritis. If these casts are very large, 
they may show amyloid degeneration of the kidney. They have 
often been wrongly called "waxy" casts. (See Plate X, Fig. 1.) 

Casts are not to be confused with cylindroids or streamers. These 
cylindroids appear in several forms. Most commonly they look like 
threads or filaments which are transparent and often somewhat 
striated or hyaline in appearance. They are often long enough to 
extend completely across the microscopic field, and if followed out 
to the end will be found to taper off or gradually become more and 




Fig. 139. — Cylindroids from albuminous urine, a, b, and c. Ribbon-like forms, d. Cast-like 
form, with cells upon its surface, e. Filamentous forms iu a clump. 



more transparent until they cannot be outlined. For this reason 
too much light should not be used in searching for them, nor should 
a lens of too high a power be used. These cylindroids often are 
grouped in bunches. In other instances we find cylindroids in the 
form of ribbons, or, in other words, they are wider than the thread- 
like masses just described. In still other instances the resemblances 
to true tube casts are so marked that a differentiation is scarcely 
possible, except that they are sometimes found to have a filiform 
tail-like ending (Figs. 139, 140, 141 and 142). The significance 
of cylindroids is not definitely known, but they may be taken as an 
indication of irritation of the kidneys, even if albumin and true 
casts cannot be found in the urine. They are often seen in the renal 



MICROSCOPIC APPEARANCE OF URINE AND ITS CONTENTS 349 



irritation following or, rather, accompanying the conditions called 
lithemia or uricemia, and in that condition in which we find oxaluria. 

According to Bramwell, the following is the best method of stain- 
ing and mounting tube casts and other urinary deposits. He uses 
picrocarmine. 

"1. An ordinary conical urine glass is filled with equal parts of 
urine and an aqueous solution of boric acid, and set aside until the 
deposit settles. 





Fig. HO. — Non-albuminous urine. 
Cast-like forms with deposit of urates. 



Fig. 141.- Non albuminous urine. 
a and b. Cast-like forms, c. Filamentous- 




Fig. 142.— Filamentous and ribbon-like eylindroids. 

"2. The deposit is then drawn off by means of a pipette, and 
transferred to an ordinary test-tube, in which a small quantity (h dr. 
is quite sufficient) of picrocarmine solution has been previously 
placed. 

"3. The urine and staining fluids are then thoroughly mixed 
by inverting the test tube tw T o or three times, the end being closed, 
of course, by the thumb. 

"4. The test tube containing the urine and staining fluid is then 
set aside to stand for twenty-four hours. 

"5. The deposit, which has by that time settled at the bottom of 



350 THE URINARY BLADDER AND THE URINE 

the test tube, is then drawn off by a fine-mouthed pipette, placed on 
a slide, covered, and examined under a low power. 

"If any tube casts are present, they are very easily detected by 
this method. 

"When a cast is detected, it should be carefully brought to the 
centre of the field and examined with a higher power. If amyloid 
degeneration is suspected, methyl violet may be used, for in some 
cases of waxy disease of the kidney the tube casts give the character- 
istic rose-pink reaction with methyl violet. For permanent prep- 
aration the deposit is drawn off as in No. 5, above, and transferred 
to a small tube of Farrant's medium, 1 in which it remains until the 
organic deposit has settled, when it is again drawn off and trans- 
ferred to clear Farrant's solution, whence it is mounted in the usual 
manner. All organic deposits are thus stained and mounted in a 
perfectly clear medium. Their minute characters can be studied 
with the highest powers of the microscope." 

The most important sedimentary substances for diagnostic pur- 
poses, other than casts, are the products of tissue changes, or are 
derived from articles of food. These substances are chiefly the acid 
urates of sodium and potassium, the alkaline urates of ammonium 
and potassium, uric acid, oxalate of lime, the phosphate, carbonate, 
and sulphate of lime, and the so-called triple phosphate (ammonio- 
magnesic phosphate). 

The discovery in a urinary sediment of fine shapeless granules, 
which occasionally may be crystalline and shaped like a fan, which 
are generally brown or pinkish in hue, indicates acid sodium urate. 
Urine containing such deposits is found to become acid on standing, 
and will form a brick-dust deposit as soon as it is cooled. Acid 
potassium urate and acid calcium urate, which occur in an amor- 
phous form, are mixed with it in smaller quantities. 

The urates themselves have no particular importance except that 
they are often present in excess in fever, wasting diseases, gastric 
disorders, and in attacks of gout. 

When in a highly acid urine the student finds rhombic or diamond- 
shaped plates (see Plate X, Fig. 2), or plates of a similar shape with 
the lateral angles rounded off, or quadrate crystals or square plates, 
or plates like double-headed arrows, or rosettes of crystals, or bundles 
of crystals like bundles of kindling wood, these forms are uric acid. 
Usually they are slightly yellow but they may be colorless. Any 
urine will deposit such crystals if it stands for many hours (say ten 
hours), as its acidity increases, and, therefore, the discovery of these 

i Farrant's solution is made as follows: Dissolve 1 gm. of arsenous acid in 200 c.c. of dis- 
tilled water. In this dissolve 130 gm. of gum acacia with frequent stirring, and add 100 c.c. 
of glycerin. Filter the solution through fine Swedish paper upon which has been deposited a 
thin layer of tajc. 



MICROSCOPIC APPEARANCE OF URINE AND ITS CONTENTS 351 

crystals only possesses significance if they are found in from four 
to six hours, as this shows an excess of uric acid, which in turn is 
found in gouty or rheumatic persons or in those who eat to excess 
and take no exercise. Often an excess of uric acid in the urine 
antedates the development of chronic contracted kidney. Uric 
acid also appears in excess in cases of fever and acute inflammations. 
It is also eliminated in excess in leukemia, splenic enlargement, 
hepatic cirrhosis, and gastro-intestinal catarrh. The rosette crystals 
just named are often found in diabetic urine. 

Small, square, brilliant octahedral crystals which are perfectly 
transparent and refract light strongly, looking somewhat like the 
back of a square envelope at times, arc those of oxalate; of lime 
(Fig. 143). The significance of oxaluria is quite important, for it 




Fig. 143. — Oxalate of lime crystals. 



is often a concomitant symptom of melancholia depending upon 
defective metabolism. The finding of oxaluria separates this class 
of cases from those of the true disease melancholia, and indicates 
the use of nitrohydrochloric acid. These crystals are, however, 
found in the urine of persons who have eaten pears, cabbage, or 
tomatoes, and in that of persons suffering from spermatorrhea. If 
not due to the ingestion of the foods named, oxaluria indicates 
deficient oxidation of nitrogenous tissues. 

Creatin in the urine occurs in very brilliant prisms of a rhomboid 
form, the end of which is often split or frayed. (See Fig. 144, a.) 
It is not present in normal urine. 

Creatinin exists in normal urine in small amounts in prismatic, 
colorless, brilliant crystals of the shape shown in Fig. 144, b. 



352 



THE URINARY BLADDER AND THE URINE 



When dark-brown spherical masses covered with thorn-like 
crystals or sharp spicules are formed in alkaline urine, they are 
composed of ammonium urate (see Plate X, Fig. 3), and they will be 
found associated with crystals which are flat or shaped like coffin 
lids, or more rarely are feathery, star-shaped masses which are large 




Fig. 144. — Crystals of creatin and creatinin. a Crystals of creatin. b. Crystals of 
creatinin. c. Crystals of chloride of zinc and creatin. (Charles.) 




Fig. 145.— Triple phosphate crystals. 

in size. These are the crystals of the triple phosphate (Fig. 145). 
In addition, such urine will contain amorphous calcic phosphate. 

The crystals of the triple phosphate are of some diagnostic impor- 
tance, as they do not exist in the normal urine, but are formed when 



MICROSCOPIC APPEARANCE OF URINE AND ITS CONTENTS 353 

ammonia is set free by the decomposition of the urea. If such crys- 
tals are found in freshly passed urine, they indicate that ammoniacal 
fermentation is taking place in the bladder, a condition often seen 
in chronic cystitis and in some cases of paraplegia arising from 
injury to the cord or myelitis. A deposit of the triple phosphate 
and amorphous calcium phosphate, making a sediment like that of 
purulent urine, is sometimes seen in persons suffering from over- 
work of the nervous system and in cases of general debility. 

In addition to these amorphous and crystalline bodies found in 
the urine there are a number of others derived from the body, or 
due to extraneous contamination. These are epithelial cells derived 
from the kidneys, ureters, bladder, or urethra. (See Plate X, Fig. 4.) 




Fig. 146. — Echinococcus, with two booklets, and section of cystic membrane, 
greatly magnified. (Peyer.) 

Eggs or bodies of several parasites, tubercle bacilli, gonococci and 
streptococci, or staphylococci are also sometimes seen under the 
microscope. In addition, we find spermatozoa in certain cases. 
(See Fig. 148.) 

Thus, we may find the embryos of filaria, echinococcus hooklets 
(Fig. 146), and the eggs of distoma hematobium, which are very 
rarely seen. 

Tubercle bacilli are to be found by the same staining processes as 
when they are sought for in the sputum (see chapter on Cough and 
Expectoration), and, if found in the urine, indicate renal or vesical 
tuberculous infection, provided that the patient has contaminated 
the vessel containing the urine by sputum infected with the organism. 
They are not to be confused with the bacilli found in preputial 
23 



3,34 



THE URINARY BLADDER AND THE URINE 



smegma, which look like tubercle bacilli and take the same stains, 
but they are differentiated by decolorizing methods. 

Gonococci indicate the presence of a specific urethritis or vagi- 
nitis, and are found by staining and using a -^ homogeneous immer- 
sion lens with a No. 2 eye piece. The process of staining is by the 
use of eosin and methylene blue. The material on the cover-glass 
is stained for a few seconds in an alcoholic solution of eosin, then 
the excess of stain is washed off, and the slide is placed for ten 

"X... 



. \JA>^ 



... 



Vs. 



Fig. 147. — Streptococci. (Abbott.) 




Fig. 148. — Spermatozoa, witb casts of seminal tubules and spermine crystals. 

minutes in an aqueous solution of methylene blue. Streptococci 
appear in chains and are stained by the same process. They show 
infection from pus and are found in cases of erysipelas (Fig. 147). 
Staphylococci also indicate pus formation in the urinary tract. 

The presence of spermatozoa is not so common as is generally 
thought. They may be in the urine either as the result of a true 
spermatorrhea, which is rare, or from some of the semen remaining 
in the urethra after an ejaculation in coitus, or from an emission at 
night without intercourse. They appear as small, transparent 



CHEMICAL TESTS 355 

bodies having a head and tail, and, if alive, possess very active move- 
ments (Fig. 148). 

Fermentation resulting from the presence of a number of special 
fungi takes place in both healthy and diseased urines after they are 
passed. In normal urines the acidity, which is generally present to 
a slight degree, becomes still more acid through the growth of a 
special fungus. This process is accompanied by the deposition 
of uric acid, acid sodium urate, and calcium oxalate, and also 
amorphous urates. After the urine is exposed still longer it under- 
goes an alkaline fermentation, and there develop in the fluid the 
Micrococcus ureas and Bacterium urccr. As a result, the urea takes 
up water and decomposes with the development of C0 2 and ammo- 
nia. No sooner is a positive alkaline reaction established than those 
ingredients of the urine which are insoluble in an alkaline solution 
are precipitated, namely, amorphous calcic phosphate, ammonium 
urate, and'ammoniomagncsic phosphate. The first is amorphous, 
but the ammonium urate appears under the microscope in the form 
of small granules of a dark color which are covered with spines. 
The crystals of ammoniomagnesic phosphate are shaped like a 
coffin lid and are large. 

The third form of fermentation taking place in the urine is that 
which occurs in diabetic urine, and is due to saccharomyces albi- 
cans, the microorganism which produces fermentation in ordinary 
solutions of glucose. 

CHEMICAL TESTS. 

The chemical tests of the urine give us much important informa- 
tion. We commonly test it for albumin and for sugar, and if we 
wish still further information, we examine it for its percentage of 
urea, peptones, chlorides, blood, and albumoses. 

Urine to be subjected to chemical examination should always be 
filtered if strictly accurate results are sought. 

Tests for Albumin. — There are several forms of albumin found 
in the urine, of which four are possessed of considerable diagnostic 
significance, namely, serum albumin and serum globulin, nucleo- 
albumin and Bence-Jones albumin or albumose. Serum albumin 
and serum globulin are the forms found in the urine in cases 
of nephritis, whereas, nucleo-albumin arises from pus or other 
causes. Bence-Jones albumin is sometimes indicative of bone tumor 
(see below). 

The tests most commonly used are the boiling test, with acidified 
urine, and Heller's, or the nitric acid test. If either of these tests 
show albumin to be present in large amounts such albumin is almost 
certainly serum albumin and serum globulin. If, however, the reac- 



356 THE URINARY BLADDER AND THE URINE 

turn is very faint it may possibly be due to nucleo-albumin, and this 
must be excluded by additional tests (see below). 

The boiling test consists in taking filtered urine and pouring 
enough of it into a perfectly clean test tube to fill it about two- 
thirds. If the urine be turbid by reason of an excess of urates, 
the fluid can be rendered clear by gently heating all of it. To 
this urine are now added a few drops of acetic acid to render it acid ; 
for if neutral, the albumin will not be coagulated by heat. The 
upper part of this urine is now boiled by holding it over an alcohol 
lamp, and if albumin is present a fine cloud will appear in the boiled 
part of the urine, while the lower part remains clear. This cloud 
may be due to albumin or to earthy phosphates. If a drop or two 
of nitric acid is allowed to trickle down the side of the tube, the 
cloud is dissipated if due to phosphates but not changed if due to 
albumin. 

If acetic acid is employed in place of nitric acid for the purpose 
of acidifying the urine, care must be taken that it is not used in excess, 
as under these circumstances the albumin will be dissolved. Indeed, 
this possibility of the solution of acid albumin is one of the fallacies 
in the boiling test which may be avoided if, after acidifying the urine 
until it is distinctly acid, one-sixth of the urinary volume of a satu- 
rated solution of common salt, sodium sulphate, or magnesium 
sulphate is added to it, when, upon boiling, the albumin is pre- 
cipitated. This test, performed with these modifications, discovers 
any albumin which may be present, even if its amount be very 
small. If upon the addition of the saturated solution of common 
salt a precipitate is formed, this may be due to the presence 
of albumoses, but the albumose precipitated is redissolved on 
boiling. 

Another useful, rapid, and moderately accurate test for albumin 
is the so-called nitric acid test: 8 to 12 c.c. of urine are placed 
in a test tube, and then a small quantity of pure nitric acid is 
allowed to trickle down the side of the tube, in which, by reason 
of its greater specific gravity, the acid passes to the bottom, the urine 
forming a supernatant layer. If serum albumin is present, a dis- 
tinct white cloud will appear in the form of a ring at the point of 
contact between the two liquids. A much more effective way of 
performing this test is to use a conical glass, somewhat like a 
sherry glass, placing in it 20 c.c. of urine, and then by means of a 
pipette, which is carried to the bottom of the vessel, allow half 
that quantity of nitric acid to escape. This modification of Heller's 
test makes a line of albumin quite readily seen. Where only a 
small quantity is present, it may be necessary to allow the two 
liquids to remain in contact for several minutes. If an excess of 
uric acid be present, five or ten minutes after the addition of the 



CHEMICAL TESTS 

nitric acid a sharply defined ring, somewhat similar to that due to 
albumin, will be found a short distance above the line of contact. 

Another way is to place the acid in the tube first and allow the 
urine to flow on it. Boston has suggested for bedside use that the 

physician dip a glass tube in the urine. The finder is placed on 
the top of the tube to prevent escape of the fluid ;h it is lifted from 
the vessel. The outer surface is wiped with a towel and the tube i- 
then immersed in a bottle of nitric acid. The finger i- removed and 
the acid pushes the urine up the tube. At the point where the two 
fluids meet in the tube the ring of albumin mav be -fen. 

The potassium ferrocyanide test for albumin consists in strongly 
acidifying a few cubic centimeter- of urine with acetic acid, and 
then adding a few drops of a 10 per cent, solution of potassium 
ferrocyanide. If albumin i- present in quantity, a flaky precipitate 
occurs. If present in minute quantity, the solution become- turbid. 
If the urine is very concentrated, it should be diluted with water 
before this test i- employed. In this test, also, the precipitate may 
be due to albumose, and it will disappear upon boiling. If the pre- 
cipitate only partially disappears, it i- fair to assume that both albu- 
mose and albumin are present. The development of a cloud in the 
urine after the acetic acid is added and before the potassium ferro- 
cyanide is used, doe- not indicate either albumose or albumin. 

The trichloracetic acid test for albumin is more delicate than any 
of those which have been described. Indeed, it is SO delicate that 
it frequently discovers albumin in urine which is certainly normal. 
By mean- of a pipette, one to two cubic centimeter- of a watery 
solution of trichloracetic acid, specific gravity 1147, are conveyed 
to the bottom of a test tube .holding several cubic centimeter- of 
urine which has been carefully filtered. If albumin is present, a 
white ring will be seen to form at the line of contact between the 
trichloracetic acid below and the urine above. This line may be 
due to albumose, but is again to be differentiated by the fact that it 
disappears on boiling if due to this substance. Sometimes uric acid 
produces a somewhat similar line to that caused by albumin, but 
it also disappears on heating, and its appearance can be prevented 
by using a urine which is fairly well diluted. 

It is to be borne in mind that one test is not exclusive in proving 
the absence of albuminuria. Several tests of different samples of 
urine are essential before the correct result is arrived at because it 
not infrequently happens that one sample may be free from albumin 
even if it is usually present. 

When nitric acid is added to the urine after it has been boiled, the 
urine sometimes becomes distinctly yellow, and, upon cooling, a 
white precipitate appears. Under these circumstances the presence 
of albumose is indicated. This precipitate is to be separated from 



358 



THE URINARY BLADDER AND THE URINE 



the dark-brown coloration sometimes due to uric acid, which develops 

after a considerable length of time in urine which has been treated 

in the manner described. 

The presence of a very faint reaction for albumin may 
be due to the presence of nucleo-albumin, which is not 
indicative of renal disease. This substance is not precipi- 
tated by heat and acid in urine having a high content of 
salt. If, therefore, after adding to the urine an amount of 
saturated sodium chloride solution equal to one-fifth its 
volume, heating and adding 2 or 3 drops of 50 per cent, 
solution of acetic acid and then heating again the cloud 
persists, this proves the presence of serum albumin and 
excludes nucleo-albumin. 

It is to be remembered that albumoses are precipitated 
by heat, but redissolved when the temperature approaches 
the boiling point. 

The Quantitative Tests for albumin are many of them 
impractical for the busy doctor. The best method is by 
means of percentage tubes placed in a centrifuge machine. 
By this means all the albumin is thrown down. The tubes 
are filled to the 10 c.c. mark with urine and 2\ c.c. of 
potassium ferrocyanide solution (one part to ten) are added. 
fig. 149. ]S[ ex t we add 1 \ c.c. acetic acid and thoroughly mix all 
u eter these liquids, and the tube being placed in the centrifuge the 
machine is worked until all the albumin has settled. Each 

-j- 1 ^ c.c. mark on the tube represents 1 per cent, by bulk of albumin; 

that is, if the albumin extends up to the 3^ c.c. mark the albumin 

amounts to 35 per cent. 




Fig. 150.— Crystals of creatinin-zinc chloride. (Salkovvski.) 

Another useful method is that known as Esbach's. A special 
test tube, known as an albuminometer, is used, on which is marked 



CHEMICAL TESTS 359 

{i letter U and a letter R (Fig. 149). The urine, which has been 
carefully filtered, is poured in the tube until it reaches the letter U, 
this portion of the tube being also provided with a scale reading 
from 1 to 7. The reagent employed is then poured in until the 
letter R is reached, when the tube is closed with a stopper, and it 
is turned up and down a number of times, so that the fluids may 
become thoroughly mixed. It is then set aside for twenty-four hours, 
when the serum albumin, serum globulin, albumose, uric acid, and 
creatinin will have been precipitated. The amount of these solids 
in grams per thousand may be then directly read off from the scale. 
The reaction of the urine to be tested should be acid, and, if necessary, 
acetic acid must be added to it for the purpose of acidifying it. 
Further, its specific gravity should not be over 100G or 1008. If the 
specific gravity is higher than this, it must be reduced by the addition 
of water. The temperature should be in the neighborhood of 70° F. 
Fsbach's reagent is composed of 10 gr. of picric acid and 20 gr. of 
citric acid dissolved in a liter of distilled water. 

The Significance of Albuminuria. — The significance of albuminuria 
is not as grave in all cases as it was considered at one time, nor is 
its quantity necessarily of great import, for in some of the gravest 
cases of renal disease, as chronic contracted kidney, it is excreted 
in very small amount, and it occurs in the urine sometimes in 
large quantities without any kidney lesion being present. As a 
rule, however, it indicates renal disease in one of its forms, pro- 
vided it is associated with other renal symptoms. It may depend 
on changes in the blood in which the divisibility of its albumin is 
increased (Semmola), and when its coagulability is diminished. 
Wright and Ross have shown that the use of full doses of cal- 
cium chloride or lactate will arrest this form of albuminuria in 
some cases. We see albuminuria in cases of anemia and in con- 
valescence from protracted illness or from the effects of poisons. 
Again, circulatory changes ma\ cause albuminuria by causing 
congestion of the kidney, as in cases of failing heart from its various 
causes. There is an intermittent, little understood form of albu- 
minuria, called cyclic albuminuria, orthostatic albuminuria, or the 
albuminuria of adolescence, in which the albumin is absent on rising 
from bed in the morning, but appears if exercise is taken. An 
excess of albumin in the diet may cause albuminuria, which is not 
necessarily indicative of renal disease. Traces of albumin may be 
due to the presence of a little pus arising from cystitis or urethritis, 
or from a vaginitis. In the presence of albuminuria the real test to 
determine the presence of actual kidney disease rests upon the dis- 
covery of casts -on microscopic examination, but even the absence 
of casts does not negative the possibility of nephritis, for they may 
be absent, yet renal disease be present. 



360 THE URINARY BLADDER AND THE URINE 

Tests for Blood. — A test which can be most easily applied to deter- 
mine the presence of blood, if the microscope cannot be used, is 
Heller's test, which consists in adding to a few cubic centimeters of 
urine a little caustic soda, so as to render the liquid strongly alkaline. 
The urine is now heated to boiling, and if blood is present a bottle- 
green color is produced , and the phosphates fall to the bottom of the 
test tube in fine flakes, tinged brownish red by the coloring matter of 
the blood. 

Still another test, and perhaps the best known to determine the 
presence of hemoglobin in the urine, is the so-called guaiacum test. 
The urine having been placed in a test tube, a mixture in equal parts 
of tincture of guaiacum and oil of turpentine, which has been ozo- 
nized by exposure to the air, is allowed to flow gently along the side 
of the tube, so as to rest upon the urine. If blood pigment is present, 
a white ring, which gradually becomes blue, forms at the point of 
contact between the two liquids. 

The best test for blood is Holland's modified guaiac test: A solu- 
tion is made of freshly broken pieces of guaiac resin by boiling 
them with alcohol in a test tube for a few minutes until the tincture 
is yellow. The suspected material, which may be a drop or two of 
blood or of bloody urine or of water in which a blood-stained fabric 
has been steeped, is cautiously mixed with a drop or two of guaiac 
solution to make a milky mixture. This is brought in contact with 
a fragment of sodium perborate on a white plate. 

If the proportion of blood is large the white perborate turns blue 
in a few minutes and remains blue until the drying of the guaiac 
leaves a yellow residue which changes the blue to green. This blue- 
green color persists on and about the perborate and is well shown 
on the white background for at least a week. If the proportion of 
blood is small the white perborate takes on a pale blue hue which 
turns green as the guaiac dries. The next day a distinct green 
stain is left on the white plate. The test is simple and delicate, 
though it must necessarily be open to the fallacies that belong to 
the guaiac test in any form. A distinct reaction was obtained from 
a small five-year-old blood-stain on linen. 

Tests for Albumose. — Albumoses in the urine may be discovered 
by the use of certain tests, but even if they are found their presence 
has no definite significance. 

Harris asserts that albumosuria is simply a manifestation of the 
action of microorganisms, and is thus only an indication of an 
infective process; but Fitz holds that its persistent presence nearly 
always points to a fatal ending. It ought not to be forgotten that 
albumosuria occurs in the normal puerperium. 

Under the name of myelopathic albumosuria, Bradshawe has de- 
scribed a very rare condition, multiple myeloma, in which, with 



CHEMICAL TESTS 361 

thinning of the bones and overgrowth of gelatinous masses in the 
cancellous tissue, there develops an extraordinary degree of albu- 
mosuria. The patient becomes exceedingly weak and feeble, and 
finally dies from exhaustion or intercurrent maladies. The pecu- 
liarity of albumosuria is that the albumose coagulates below the 
boiling point and re-dissolves on boiling. Mineral acids precipitate 
it in the cold, but boiling dissolves the precipitate. 

Tests for Peptone. — Peptonuria, at one time considered patho- 
logically identical with albumosuria, has been separated from 
the latter state by Chittenden's researches. It is discovered by 
saturating the urine, which has been first slightly acidified with 
acetic acid whilst boiling, with ammonium sulphate, and filter- 
ing out any precipitate. If the filtrate contains a substance 
which is precipitated by potassiomercuric iodide 1 or picric acid, it is 
peptone. Peptone is not precipitated by saturation with ammo- 
nium sulphate, and albumose is precipitated by it. Pepton- 
uria is present in croupous pneumonia, all suppurative processes, 
empyema, tuberculosis, smallpox, mumps, erysipelas, cancer of the 
viscera, jaundice, and apoplexy, and in typhoid fever and phos- 
phorus poisoning. Von Jaksch asserts that it is present in epidemic 
cerebrospinal meningitis and absent in tuberculous meningitis, and 
that it is a positive differential sign of the former disease if no ulcera- 
tion of the lungs is present. In the presence of acute inflammations 
the development of peptonuria indicates suppuration. 

Tests for Sugar in the Urine. — The presence of sugar is determined 
by a large number of qualitative and quantitative tests, of which the 
simplest and most reliable are Haines' test and the test of Whitney. 
Haines' test consists in making a solution as follows: pure copper 
sulphate, 30 gr. ; distilled water, \ oz. ; thoroughly dissolve the cop- 
per salt in the water; add pure glycerin, \ oz., which is to be 
thoroughly mixed; and then add liquor potassse, 5 oz. One dram 
of this is to be placed in a test tube and gently boiled, and to 
this are added 6 to 8 drops of the urine, and the liquid again 
gently boiled. If sugar is present, a copious yellow precipitate is 
formed. This is better than Fehling's test, because it is a perma- 
nent fluid. 

Whitney's test is a solution of ammoniocupric sulphate, of which 
1 dr. is decolorized by -^ gr. of glucose. The solution of the 
amount of 1 dr. is placed in a test tube and heated to the boil- 
ing point. The urine is now added drop by drop. If no sugar 
is present, no change will occur; but if it is, the blue color will 
begin to fade, and finally the liquid will become perfectly colorless. 
As the fading process begins the urine should be added more slowly, 
three to five seconds of boiling intervening between each drop. If 
there is any shade of blue or green left in the solution, reduction 



302 THE URINARY BLADDER AND THE URINE 

has not taken place. The following table shows how this test may 
be used for the quantitative estimation of sugar: 

// reduced by It contains to the ounce. Percentage. 

1 drop 16 or more grains. 3.33 

2 drops 8 1.67 

3 " . . . . . . . 5.33 1.11 

4 " . . . . . . .4 0.83 • 

5 " ' . . . . " . . . 3.20 0.67 

6 " 2.67 0.56 

7 " ....... 2.29 0.48 

8 " 2 0.32 

9 " 1.78 0.37 

10 " 1.60 0.33 

If the urine contains more than 3.33 per cent, of sugar, it is 
to be diluted by from 1 to 10 parts of pure water, and the amount 
found in the table multiplied by the amount of dilution. Usually 
diabetic urine contains not less than i of 1 per cent, and rarely 
more than 1 per cent. This test is not reliable if the solution is not 
freshly prepared. 

As Fehling's test is so widely used it must be mentioned. Wick- 
ham Legge thus describes it: 

This solution may be prepared in the following way: 665 \ gr. 
of crystallized potassiotartrate of sodium are dissolved in 5 fl. 
oz. of a solution of caustic potash, sp. gr. 1120. Into this 
alkaline solution is poured a fluid prepared by dissolving 133^ gr. 
of sulphate of copper in 10 fl. dr. of water. The solution is 
exceedingly apt to decompose, and must always be kept in stoppered 
bottles and in a cool place. It is usually, therefore, more convenient 
not to mix the alkali and copper until the solution is wanted for use. 
In this case 1 fl. dr. of the sulphate of copper solution may be 
added to \ fl. oz. of the alkaline solution prepared as above. 

About 2 drams of this test solution are poured into an ordinary 
test tube, and the fluid boiled over a lamp and set aside for twelve 
hours. If no deposit forms, the solution may be used for analysis; 
but if a red precipitate be thrown down, the liquid has decomposed, 
and a fresh supply must be had. 

While the solution is boiling in the test tube the urine must be 
added to it drop by drop, and the effect watched. A few drops of 
a sample of urine which contains a large percentage of sugar will at 
once give a precipitate of yellow or red suboxide of copper; but if 
no precipitate occur, the urine should be added to the fluid drop by 
drop, any deposit being carefully looked for, until a quantity equal 
to that of Fehling's solution employed has been added. If on 
precipitate be found after setting the test tube aside for an hour, 
the urine may be considered free from sugar. 

Cautions: 1. The test solution should never be used without boil- 



CHEMICAL TESTS 303 

ing beforehand for a few seconds, the tartrate being exceedingly apt 
to decompose, and the solution then reduces copper as effectually as 
would grape sugar. 

2. The quantity of urine used in the test should never be greater 
than the quantity of test solution employed. 

3. After boiling urine in volume equal to Fehling's solution, the 
boiling of the mixture must be discontinued, as other bodies present 
in the urine, besides sugar, will reduce copper at a high temperature. 

If the examination for sugar is to be made with the greatest care, 
the urine should always be filtered, at least three times, through 
animal charcoal. This removes all urates and uric acid, which often 
partly reduce the Fehling's solution, but the sugar goes through the 
filter. 

Sir William Roberts directed that Fehling's solution be placed 
in a test tube to the depth of about one-quarter inch and the filtered 
urine added to the depth of two inches, and the two fluids well 
mixed. The flame of the lamp is then applied to the upper part of 
the urine, as in testing for albumin, and this is briskly boiled for a 
few seconds. The test tube is now held up to the light, and, if 
sugar is present, the upper part has a yellowish tinge, while the 
earthy phosphates are thrown down in golden-colored flocculi. 

Trommer's test for sugar consists in strongly alkalinizing a few 
cubic centimeters of urine with a solution of sodium hydrate, and 
then adding drop by drop a 5 per cent, solution of sulphate of copper 
until the cupric oxide formed is no longer dissolved. The mixture 
is then carefully heated, and if sugar is present, a yellow precipitate 
of cuprous oxide is formed which gradually settles to the bottom of 
the test tube as a red sediment. 

The phenylhydrazin test consists in adding to 6 or 8 c.c. of urine 
two small pinches of phenylhydrazin hvdrochlorate equalling about 
5 to 7 gr., and 15 gr. of acetate of sodium. This mixture is then 
warmed until the salts have been dissolved, a little water being 
added, if necessary, to aid their solution. The test tube is then 
placed in boiling water for twenty to thirty minutes, and then trans- 
ferred to a vessel containing cold water, when, if sugar is present in 
considerable quantity, a bright-yellow crystalline deposit will at 
once be thrown down and partly adhere to the tube. These crystals 
are composed of phenylglucosazon and are insoluble in water. This 
is less open to fallacy than any other test for sugar. 

The quantitative estimation of sugar is best made by the Whitney 
test, already described, or by the fermentation method of Roberts, 
which depends upon the principle that grape sugar is decomposed 
into alcohol, carbon dioxide, etc., by the fermentation set up by yeast. 
As a result of this the urine loses its specific gravity, and each degree 
of specific gravity has been found to equal 1 grain of sugar in the 



3G4 THE URINARY BLADDER AND THE URINE 

fluidounce. In other words, if the specific gravity before the test 
was 1035 and after the test 1015, the amount of sugar present would 
be 20 gr. per ounce. Four ounces of urine are placed in a twelve- 
ounce bottle and a lump of German yeast added. The bottle is 
then corked with a perforated cork to permit the gas to escape, and 
kept in a warm place for twenty-four hours. By its side is placed 
a tightly corked bottle of the same size, holding 4 oz. of urine and 
no yeast. The specific gravity of both specimens is taken simulta- 
neously, and the difference in degrees represents the number of 
grains of sugar in each ounce. The loss in degrees of specific 
gravity multiplied by 0.23 will give the percentage of sugar. 

The Significance of Sugar in the Urine. — The significance of sugar 
in the urine is various. If it is persistent and accompanied by 
wasting, polydipsia, and polyphagia, it is a sign of diabetes mellitus. 
If diabetes mellitus occurs in a young person, the prognosis as to life 
is nearly always fatal; if in middle age, it is hopeful; if in persons 
after fifty, it is quite favorable. 

Sugar is sometimes found in small amounts in the urine of very 
obese persons, and its presence under these circumstances does not 
necessarily indicate a grave prognosis; but, on the other hand, there 
are cases of so-called diabetogenous obesity in which the prognosis 
is very grave. True diabetes mellitus is to be separated from cases 
of glycosuria by the fact that the systemic symptoms of wasting, 
depraved nutrition, itching, furunculosis, and profuse diuresis are 
present. Diabetes occurring in old age, or after sixty years of age, 
has not the grave prognosis attached to it that exists in connection 
with the disease in earlier life, as just stated. The younger the 
patient the graver the malady. (See also the end of this chapter.) 

The indications of glycosuria, aside from diabetes mellitus, are 
of little importance. Glycosuria occurs in the course of conval- 
escence from many infectious diseases, particularly typhoid fever, 
measles, scarlet fever, diphtheria, influenza, and malarial disease; 
after cerebral hemorrhage and nervous injuries, and after the inges- 
tion of some poisons, notably phloridzin, chloral, arsenic, alcohol, 
and curare. It also sometimes occurs as a result of the ingestion of 
large amounts of sugar and starchy foods in persons who are unable 
to digest and assimilate carbohydrate foods in excess. Unless 
the glycosuria is associated with the other symptoms of diabetes 
mellitus, it is not a positive sign of the disease, for glycosuria is a 
symptom of a number of states other than diabetes mellitus, as has 
just been pointed out. Pentosuria, or the presence in the urine 
of an optically inactive sugar which does not ferment with yeast, is 
a rather rare condition which in nearly every case has been mistaken 
for diabetes. This urine reduces Fehling's solution, but in an un- 
usual way, the fluid remaining clear a short time and then suddenly 



CHEMICAL TESTS 365 

changing color throughout. The orein test practically identifies the 
pentoses, but complex chemical methods are needed absolutely to 
verity the diagnosis. In the cases studied the condition appear^ to 
have been relatively harmless, though its true significance is not as 

yet fully understood. The dietetic treatment of glycosuria has no 
effect upon it, hence the importance of differentiating between it and 
glycosuria. 

Finally, it is not to be forgotten that a condition known as a/l:ap- 
tonuria may exist. In this state the urine reduces alkaline solutions 
of copper, and on exposure to the air absorbs oxygen in the presence 
of an alkali and becomes of a dark-brown or black hue. The specific 
gravity of the urine is low, 1014 to 1020, and there is no marked 
polyuria. While such a urine reduces Fehling's solution, it will not 
give the reaction with the bismuth, the phenylhydrazin, the fer- 
mentation, or polariscope tests for sugar. This condition of alkap- 
tonuria has no direct pathological significance so far as is known. 
It is often found in several members <>f the same family. 

Tests for Acetonuria. — The presence of an excess of acetone in 
the urine in association with glycosuria is diagnostic of true diabetes 
mellitus, and if the acetone is present in large quantity, the condition 
may be considered as grave. 

The best test for acetone, in that it is the simplest, is Oppen- 
heimer's modification of DennigeV test. It is carried out as fol- 
lows: The reagent named below is added drop by drop to about 
3 c.c. of urine until the precipitate which is formed no longer dis- 
appears on stirring. A few more drops are now added, and 
after several minutes the precipitate i- filtered off. The clear 
filtrate now has added to it 2 c.c. of the reagent and 4 c.c. 
of a 30 per cent, solution of sulphuric acid, and is boiled for 
a minute or placed in a water-bath of boiling water. If acetone is 
present in large quantity, a heavy white precipitate forms at once; 
while if it is present in minute quantity, a slight cloud develops on 
standing after several minutes. The precipitate is almost completely 
dissolved by adding an excess of hydrochloric acid. It is claimed 
that this test will reveal acetone in the presence of 1 to 5000. If 
albumin is present in the urine, large amounts of the reagent must 
be added. The reagent consists of 20 grams of concentrated H.,S( ) 

l> O 2 4 

added to 100 c.c. of distilled water, to which are also added 5 grams 
of freshly prepared yellow oxide of mercury. 

Tests for Indican. — An excess of indican in the urine possesses 
considerable clinical significance. It nearly always indicates putre- 
factive processes going on in the intestine, probably resulting from 
the putrefaction of albuminous foods. A certain amount of indican 
is always present in the urine, particularly if large quantities of 
animal food have been taken, and in the presence of intestinal 



366 THE URINARY BLADDER AND THE URINE 

obstruction it often appears in the urine in very large quantities, 
so that its presence in excess has been considered as a valuable 
aid to the diagnosis of this condition, since in ordinary constipa- 
tion it does not appear in great excess. 

The test for indican is performed by means of the rrethod of 
Jarre*, as modified by Stokvis, as follows: Equal parts of urine and 
concentrated hydrochloric acid are placed in a test tube, and to 
this mixture are added 2 or 3 drops of a strong solution of sodium 
hypochlorite. To this are also added 1 to 2 c.c. of chloroform, and 
the mixture is then thoroughly shaken. The indigo which is set 
free is taken up by the chloroform, which becomes blue to a greater 
or less extent according to the quantity of indican which is present. 
The fallacies connected with this test are : First, that bile pigment 
interferes with it. If bile pigments are present in considerable 
quantity, they must be removed by the previous addition to the urine 
of a solution of subacetate of lead in moderate quantity. The pres- 
ence of iodine, due to the use of potassium iodide, will also color the 
chloroform red instead of blue. 

My colleague, Dr. Holland, has suggested the following test as 
more reliable: To a test-tube filled one-fourth with urine an equal 
quantity of concentrated hydrochloric acid is added to liberate the 
indoxylsulphuric acid or urinary indican and then as oxidizer a 
piece of sodium perborate as large as a full-sized pea. The mixture, 
which immediately effervesces briskly, is gently agitated to dissolve 
the perborate. The urine promptly deepens in color, and if the 
amount of indican be large, turns faintly blue. To concentrate the 
color, 1 c.c. (16 minims) of chloroform is added, the tube is closed 
with the thumb and the contents gently shaken for at least two 
minutes. The chloroform separates at the bottom as a layer varying 
in depth of blueness with the proportion of indican. Some patho- 
logical urines yield a layer almost black in color. If the shaking is 
too vigorous the chloroform is emulsified and remains milky, though 
with a decided blue tinge. 

Test for Bile. — The best test for bile in the urine is Gmelin's test, 
as modified by Rosenbach. After the urine has been filtered through 
thick filter paper, the paper, still wet, is removed from the funnel, 
and a drop of concentrated nitric acid is allowed to touch its inner 
surface, when if bilirubin is present, a play of colors will take place 
at the line of contact, the green color being most typical. 

The Urea in the Urine. — The amount of urea is to be estimated 
by the process of Lyons, as follows (Fig. 151 ): 1 

1. A bottle is provided with a perforated rubber cork and delivery 
tube; in this the decomposition of the urea is effected. 

1 This apparatus, with fall directions for use, can be obtained from Parke, Davis & Companr, 
Detroit, Mich., for one dollar. 



CHEMICAL TESTS 



367 



2. A small test tube to contain the urine, graduated to hold 4 c.c., 
the quantity employed in each experiment. 

3. A graduated jar for measuring the gas evolved. The jar is 
provided at the bottom with an "overflow" tube, and at the top 
with a vent tube closed with a rubber cap, to secure accurate adjust- 
ment of the level of the fluid in the jar at the commencement of the 
experiment. 

The process is as follows: put into the square bottle 20 c.c. of a 
special solution of chlorinated soda (for formula see below), and add 
5 c.c. of a 20 per cent, solution of potassium bromide; fill the test 
tube exactly to the mark (4 c.c.) with the urine to be examined, and 
lower it into the bottle by means of a thread or by the aid of a pair 
of dressing forceps, taking care that none of its contents is spilled 
in the operation. Fill the graduated jar with water, which must be 
of the same temperature as the air of the room, to a point a little 
above the 0° of the scale, supporting the extremity of the overflow 




Fig. 151. — Ureometer. 



tube so that no water can escape. Remove the rubber cap from the 
vent tube and connect the apparatus, pressing in the rubber stoppers 
firmly so as to make the joints air-tight. Finally, put on the rubber 
cap, drawing it down so as to force a little water out of the overflow 
tube, and bring the level of the water remaining exactly to the 0° 
mark, the orifice of the overflow tube being on the same level. A 
little practice will make this easy. 

To make sure that the connections are all perfectly air-tight, lower 
the end of the overflow tube a few inches; a few drops of water will 
escape from diminished pressure, but if the joints are perfect there 
will be no further dropping. If there is any leakage, the defective 
joint must be found and the difficulty corrected before proceeding 
farther with the experiment. Having made sure that the connec- 
tions are perfect, catch the curved end of the overflow tube over the 
edge of a measuring graduate, as shown in the illustration (an ordi- 
nary bottle or any other receiver may be used in place of the grad- 
uate). Now, by canting the bottle, cause the urine to flow out of 



368 



THE URINARY BLADDER AND THE URINE 



the test tube and mix the test solution. Effervescence is at once 
produced, and the gas evolved forces a corresponding volume of 
water out of the overflow tube. Shake the bottle occasionally to 
promote the escape of the gas. When the action appears to be at an 
end pour into the measuring graduate enough water to reach above 
the opening of the overflow tube, in order that cooling of the gas 
evolved, which at first is quite warm, may not draw air into the appa- 
ratus. Let the apparatus stand fifteen or twenty minutes to cool, 
then shake the bottle containing the urine once more and proceed 
to read off the result. To do this, it is necessary to bring the opening 
at the end of the overflow tube just to the same level as that of the 
fluid remaining in the graduated cylinder, since raising or lowering 
the tube slightly affects the volume of the gas to be measured. The 
percentage of urea is read off without need of any calculation from 
the scale of the instrument. The accompanying table will enable 
the physician to ascertain from the percentage amount of urea in the 
specimen examined what is the absolute amount of that compound 
excreted during the day, provided, of course, the whole of the urine 
passed during the twenty-four hours has been collected and care- 
fully measured. 



Per cent, of 


Quantity of 


Per cent, of 




Quantity of 


urea of 


urea in grains 


urea by urea in grains 


ureometer. 


in 1 fluidounce. 


ureometer. in 1 fluidounce 


0.1 . '■■ . 


0,456 


1.9 8.658 


0.2 


. . . 0.911 


2.0 








9.114 


0.3 


. ■ . 1367 


2.1 








9.570 


04 


1.823 


2.2 








10.025 


0.5 


2.279 


2.3 








10.481 


0.6 


2.734 


2.4 








10.937 


0.7 


3.190 


2.5 








11.393 


0.8 


3.646 


2.6 








11.848 


0.9 


4.101 


2.7 








12.304 


1.0 


4.557 


2.8 








12.760 


1.1 


5.013 


2.9 








13.215 


1.2 


5.468 


3.0 








13.671 


1.8 


5.924 


31 








14.127 


1.4 


6.380 


3.2 








14.582 


1.5 


6.836 


3.3 








15.038 


1.6 


7.291 


3.4 








15.494 


1.7 


7.747 


3.5 








15.950 


1.8 


8.203 













Example.— The patient has passed 24 fluidounces of urine, found to contain 2.4 per cent, of 
urea. The total urea excreted will therefore be 10.937 (from the table) X 24 = 262.488 grains. 

For exact estimations the temperature of the room in which the 
experiment is made must be about 70° F. (21° C). A variation 
from this temperature of 20° will, however, made a difference in the 
result of only about 0.2 per cent., so that the temperature correction 
may be regarded as unimportant. 

In the process given for the manufacture of the test solution the 
hypochlorite is changed into hypobromite. 



CHEMICAL TESTS 369 

This mixture gives more uniform and trustworthy results than 
those obtained with the chlorinated soda alone, which is recom- 
mended by Dr. Squibb. It is, in fact, identical in its action with 
the hypobromite solution, without the great inconvenience of hand- 
ling bromine. A few minutes must be allowed to elapse after the 
mixture is made before mixing the urine with it; but this need occa- 
sion no delay, since the mixture can be put into the bottle before 
filling the cylinder and making the connections. 

The activity of the solution of chlorinated soda can be easily 
tested by adding to a little of it in a test tube a few drops of the 
solution of potassium bromide, and then a little muriate of ammo- 
nium, which should cause brisk effervescence. If this is not the 
case, it is too much deteriorated for use. 

In some rare instances it will happen that the urine contains a 
larger proportion of urea than the ureometer is capable of indicating. 
When this is the case, and in general when the specific gravity of 
the urine exceeds 1.030, sugar being absent, it will be best to dilute 
the urine with an equal volume of water before making the test. 
4 c.c. of the diluted urine will then be used as usual in the experi- 
ment, but the percentage given by the reading of the instrument 
must be multiplied by 2. 

It will be found in practice that an estimation of urea by this 
apparatus consumes very little time, and the results for all practical 
purposes are as accurate as could be wished. 

Formula for Special Solution of Chlorinated Soda. — Shake chlori- 
nated lime (best quality) 12 gm. with water 100 c.c; let settle 
and filter into a 250 c.c. bottle. Wash the residue with enough 
water to obtain 130 c.c. of clear filtrate. 

Dissolve sodium carbonate 24 gm. in water 45 c.c. Add this 
solution to the above filtrate, mix thoroughly, and, when reaction is 
complete, filter, passing, if necessary, enough water through residue 
on filter to obtain 165 c.c. of filtrate. 

The estimation of the daily excretion of urea is of some value 
as an index of the activity of the kidney in the various forms of ne- 
phritis, in diabetes mellitus, during pregnancy or in the puerperium, 
and before surgical operations. The results, however, are not con- 
sidered of as great importance as formerly for it has been found 
that actual renal disease may be well advanced, and yet a high per- 
centage of urea may be present because the portion of the kidney 
which is affected may not be that which is concerned in the elimi- 
nation of this substance. The quantity of urea excreted in twenty- 
four hours is increased in nearly all fevers and inflammations, and 
is decreased in many cachectic states in which the metabolic changes 
in the tissues are impaired. It is also decreased in diseases which 
greatly modify the activity of the liver, the gland which forms urea. 
24 



370 THE URINARY BLADDER AND THE URINE 

The finding of a low percentage of urea indicates that the kidneys are 
probably made to eliminate other substances which are toxic and 
conversely, the finding of a percentage which is approximately normal 
does not necessarily prove that the function of these organs is perfect 
so far as the elimination of toxic materials is concerned. (For the 
estimation of urea, see early part of this chapter.) A persistent 
scanty urea elimination is, however, of considerable indicative value. 

Although the quantity of urea varies very greatly in' perfect 
health, the mean amount excreted in twenty-four hours by a healthy 
man of twenty to forty years is about 512 grains. Women excrete 
a little less than men, and children still less in actual quantity, but 
more in proportion to their weight. 

It is absolutely necessary in estimating the amount of urea ex- 
creted in twenty-four hours to test a sample of the urine obtained 
from all the quantity passed in that time, as a test of the urine passed 
on one occasion is no guide for the total daily quantity. 

Chlorides in the Urine. — The urine in health contains chlorides of 
sodium and potassium, and these are to be discovered by placing a 
fluidrachm of urine in a test tube and then adding a drop of nitric acid, 
and finally a few drops of a solution of nitrate of silver. If chlorides 
are present in considerable quantity, a white precipitate of chloride 
of silver is thrown down, which can easily be distinguished from 
albumin; but if some doubt is felt as to its character, the addition of 
a little caustic ammonia will redissolve it if composed of chlorides, 
and it will be reprecipitated if nitric acid is again added. If the 
same quantities of urine and reagents are taken daily and placed 
in a test tube of equal dimensions and the precipitate allowed to 
settle for twenty-four hours, we can gain an approximate estimate 
of the relative quantity of the chlorides. The amount ordinarily 
passed in twenty-four hours by a healthy man is 250 grains. 

The clinical significance of a decrease in the chlorides is not great. 
They are decreased in the acute stages of croupous pneumonia, acute 
articular rheumatism, and some other fevers; and if they gradually 
increase, they indicate the development of convalescence. 

Diazo-reaction. — Ehrlich has claimed that a distinct aid to the diag- 
nosis of enteric fever can be obtained by the so-called diazo-reaction 
of the urine, although it is to be remembered that this takes place 
in several other conditions of the body, notably pulmonary tubercu- 
losis, measles, diphtheria, croupous pneumonia, malaria, pyemia, 
scarlet fever, and erysipelas. It is usually present only in severe 
cases of these ailments. Further than this, Ehrlich asserts that the 
reaction is usually to be obtained from the fourth to the seventh day 
of the disease. So far as constancy is concerned it appears more 
frequently than the Widal reaction. A faint reaction is indicative 
of a mild attack. 



SYMPTOMS ASSOCIATED WITH URINARY DISORDERS 37] 

The test is as follows: 

(1)2 gm. (30 gr.) of sulphanilic acid, 50 c.c. of hydrochloric 
acid, and 1000 c.c. of distilled water. (2) A solution of sodium 
nitrite in water of the strength of 0.5 per cent. Fifty parts of 
No. 1 and one part of No. 2 solution are now placed in a test 
tube and an equal amount of urine added, and this mixture is 
then rendered strongly alkaline by strong ammonia-water. If the 
diazo-reaction is present, the liquid becomes pink in color; and if 
the test tube is shaken, this color is seen in the foam. Indeed, it 
is this color of the foam which is the determining factor, for this 
coloration is the point in the reaction. If the liquid only is red, 
the test is not positive. After standing a day a green precipitate 
will form in the tube, and this is very confirmatory of the presence 
of typhoid fever. 

Greene has shown that the diazo-reaction will take place in typhoid 
fever when the dilution is 1 to 100 or 1 to 150, and that this rarely, if 
ever, occurs in tuberculosis. By means of this dilution, therefore, 
additional points in differential diagnosis can be obtained. 

The diazo-reaction can also be used as a differential agent in sepa- 
rating measles from rotheln, for it does not occur in the urine in the 
latter malady. It is of value as a prognostic agent in pulmonary 
tuberculosis, because it does not appear, as a rule, until the disease 
is far advanced, and life rarely lasts more than six months after it 
appears. 



THE GENERAL SYMPTOMS ASSOCIATED WITH URINARY 
DISORDERS. 

Having considered the pathological changes found in the urine 
and their significance, we now pass on to a consideration of the gen- 
eral symptoms which will usually be found associated with these 
variations from the normal functional activity of the urinary organs. 

Let us suppose that a patient presents himself complaining that 
he has been seized with pain in the small of the back, and perhaps 
by nausea and chilly sensations, followed by a marked decrease in the 
quantity of urine secreted, which decrease may actually amount to 
suppression of the urine. The urine that is passed is high-colored 
or smoky in hue, sometimes looks like porter, and forms a very 
heavy sediment on standing. If it is filtered and tested for albumin, 
it will be found to contain this abnormal ingredient in large amount, 
and a microscopic examination of the sediment will reveal a large 
number of blood corpuscles, epithelial cells, and casts made up 
of blood cells, epithelium, and albumin. Scarcely will these signs 
have been noted when the patient will be seen to be anemic and 



372 THE URINARY BLADDER AND THE URINE 

puffiness of the face about the eyes will be evident. This puffi- 
ness may then pass on to a general anasarca, but it is to be remem- 
bered that the most violent acute diffuse nephritis may exist without 
developing anasarca. If the disease be in a child and it is due to 
scarlet fever, anasarca is common, as is also uremia. The pulse in 
patients with this form of nephritis is usually hard and tense, and the 
sharp and clear sound of the aortic valves, as heard at the second right 
costal cartilage, will indicate the high arterial tension. The skin is 
generally dry, and, it may be, harsh to the touch. Should the symp- 
toms persist for over a month the possibility of the disease becoming 
chronic renders the prognosis doubtful; but, as a rule, particularly 
in young persons, the prognosis of acute diffuse nephritis is favorable. 
In the acute diffuse nephritis of pregnancy the prognosis is, of course, 
grave if the pregnancy continues. The history of a case prior to 
the attack of acute diffuse nephritis will usually be that the patient 
has been exposed to cold or wet, has been or is a sufferer from an 
acute infectious disease, has swallowed or inhaled some irritant 
poison, or has suffered from some severe burn of the surface of the 
body. 

If, instead of an acute attack of illness, the symptoms just de- 
scribed come on gradually and insidiously, and the tendency to 
anasarca is marked and persistent, we have before us a case of 
chronic parenchymatous nephritis, in which the prognosis is most 
grave. Uremia, vomiting, and coma may occur in this class of 
patients. (See chapter on Vomiting.) Blood cells are also found in 
the sediment of the urine in these cases, but are not so numerous as 
in acute diffuse nephritis. 

A group of symptoms which differ very markedly from those just 
described occurs in cases of chronic contracted kidney (chronic inter- 
stitial nephritis). The following description of the symptoms may 
be taken as representing a typical case: the patient, who is usually 
past middle life, finds that he or she urinates more frequently and 
passes a greater amount of urine than heretofore. Often the sleep 
is disturbed by the necessity of arising to urinate. Instead of the 
urine being heavy and clouded, it is unusually clear and limpid; 
and in place of the high specific gravity of diffuse parenchymatous 
nephritis, we find it unusually low (only 1.010 to 1.015). Albumin 
is found only inconstantly and in traces, and is generally to be sought 
for in the urine passed by the patient when first arising from bed. 
The pulse is usually much increased in tension, and atheroma of the 
bloodvessels is more or less marked. This high-tension pulse is a 
valuable diagnostic sign. The heart, which in acute diffuse neph- 
ritis may be slightly dilated, or in chronic parenchymatous nephritis 
somewhat hypertrophied, is in this disease usually markedly hyper- 
trophied, and the second sound at the second right costal cartilage is 






SYMPTOMS ASSOCIATED WITH URINARY DISORDERS 373 

commonly accentuated. In addition to these symptoms we find that 
chronic bronchitis is not rare, and that pulmonary edema and attacks 
of shortness of breath, which may be called asthmatic, are often 
present, the latter being most marked at night. Uremic symptoms 
are more commonly seen in this class of cases than in any other, 
and violent vomiting, difficult of control, should always make the 
physician test the urine to discover renal mischief. Unlike parenchy- 
matous nephritis, dropsy is a rare complication of chronic contracted 
kidney. Microscopic examination of the urine will reveal only a 
few hyaline and granular casts. The prognosis as to cure is bad, 
but life may be prolonged indefinitely. 

Let us suppose, however, that a patient comes to us with a history 
of exceedingly copious urination, of great thirst, of loss of flesh, 
and has a dry, harsh skin, we immediately recognize that a test of 
the urine will probably reveal the case to be one of diabetes mellitus. 
This will be pointed to if a high specific gravity is found present in 
a clear limpid urine, and confirmed if the tests for sugar already 
given produce a reaction. The other prominent symptoms of dia- 
betes mellitus are furunculosis, intense itching and erythema (see 
chapter on the Skin), an excessive appetite, and, in some severe cases, 
gangrene of the extremities or diabetic coma (see chapter on Coma 
and Unconsciousness). If the urine has a constant low specific 
gravity and contains no albumin or sugar, the case is probably one 
of diabetes insipidus. 



CHAPTER XII. 

THE BLOOD. 

The various forms of red and white corpuscles — Their proportionate number 
in health and disease — Alterations in their form and character — The 
hemoglobin of the blood in health and disease — The various forms of 
anemia — Leukemia and pseudoleukemia — Parasites of the blood — The 
blood in typhoid fever and diabetes. 

As already pointed out in the chapter devoted to the skin, marked 
changes in the blood speedily produce manifest alterations in the 
appearance of the patient. The present chapter will be devoted to 
a consideration of the changes in the blood seen by the naked eye or 
by the aid of various forms of delicate apparatus designed to furnish 
accurate information. Before studying the conditions of the blood 
which are found in disease, it is well briefly to rehearse the character- 
istics of normal blood when it is examined outside the body. 

The blood consists of a liquid basis or plasma, in which are found 
two varieties of cells — the red blood cells, or erythrocytes, and the 
white blood cells, or leukocytes. The red cells are biconcave disks, 
dark at the edges, and with a clear or bright spot in the centre, due 
to their biconcavity. They are non-nucleated. The red color of 
the blood is due to the aggregation of immense numbers of these 
bodies, the coloring matter of which is called hemoglobin, though 
the individual corpuscle when placed in a bright light on the stage of 
the microscope appears a pale greenish yellow. The number of 
red blood cells is about 5,000,000 to the cubic millimeter of blood 
in a healthy adult male, though counts above this, even to 5,500,000, 
are not infrequent, and about 4,500,000 are present in the healthy 
female. If this number is exceeded the condition is called polycy- 
themia; if decreased, oligocythemia. 

The proportion of the white to the red cells in health is about 1 to 
500 or 600, but very great variations occur. Thus, after meals the 
white corpuscles are always increased, so that the proportion may be 
1 to 350 of the red cells. Hirt found before breakfast the proportion 
to be 1 to 716; one hour after breakfast, 1 to 347; three hours after 
breakfast, 1 to 1514; ten minutes after dinner, 1 to 1592; half an 
hour after dinner, 1 to 429; two and a half hours after, 1 to 1481; 
half an hour before supper, 1 to 544; and two hours after supper, 
1 to 1227. It is important to remember this influence of food on the 
leukocyte count. Not only may this cause produce great altera- 



MICROSCOPIC .EXAMINATION OF THE BLOOD 375 

tions in the results obtained in a blood examination, but many 
others must be considered, it being always borne in mind that 
there are pronounced variations in the blood within healthy limits, 
both in quantity, quality, and corpuscular elements. For these 
reasons slight variations should not be given much weight unless by 
repeated tests they are found constant. It is usually unsafe to rest 
upon a single test. Thus sweating, if profuse, may cause such a 
concentration of the blood that a normal number of red cells to a 
cubic millimeter may be shown when in reality there is marked 
anemia. So, too, tapping an effusion, or the use of an active hydra- 
gogue cathartic, or profuse diarrhea may cause great concentration. 
Blood obtained from a cold ear or a cold finger tip, or from these 
parts when made unduly warm by friction or heat, gives erroneous 
ideas of the state of the blood in general. 

Proceeding, then, to the study of the blood for diagnostic purposes, 
we examine it by the microscope, and by color tests. The object 
of the microscopic examination is to determine the quality and 
character of the red and the white corpuscles, their number, and the 
presence of parasites. The color tests are for the purpose of deter- 
mining the proportion of hemoglobin, or, in other words, the ability 
of the corpuscles to carry oxygen to the tissue-. 




Fig. 152.— -Stewart's forceps for holding cover-glass. 

Microscopic Examination of the Blood, — To study the blood 
microscopically we need, for ordinary corpuscular work, a quarter* 
inch or, better, a fifth- or sixth-inch objective, or, as they say on the 
Continent of Europe, a Number 7 Hartnack or a D Zeiss; and for 
examinations for parasites a T V oil-immersion lens for use with a 
condenser. The eye pieces used are generally Nos. 1, 2, and 4. 

Perfectly clean cover-glasses and slides, such as are used inordinary 
microscopic work, are also needed. It is of the greatest importance 
that these glasses shall not only be free from dust and dirt, but also 
that they shall not be finger-marked. After ordinary washing they 
should be washed in ether and alcohol, or acid alcohol, and then 
carefully dried by gauze or lint-free tissue paper. They are further 
improved by being passed a time or two through an alcohol or gas 
flame. The operator should use a pair of fine forceps provided with 
a clip, so that he can pick up a cover-glass without touching it with 
his fingers and lav the glass down without releasing: it from the 
forceps (Fig. 152), or handle them by the edge only. 



376 



THE BLOOD 



The tip of the finger or the lobe of the ear is now washed clean 
with alcohol and dried very gently, so as not to cause an artificial 
hyperemia, and the skin of the part is then punctured by a tenotome 
or a small spear point made for the purpose (Fig. 153). The first 
drop of blood which escapes is wiped off, and the centre of a cover- 
glass is touched to the second drop, so that a small amount adheres to 




Fig. 153. — Lance for stabbing skin of tip of finger or lobe of ear to obtain drop of blood. 

the surface. It is then placed with the blood side down on a clean 
glass slide, which has been slightly warmed, and examined under 
the microscope. This procedure is invaluable in the study of 
parasites, but gives so crude an idea of the true state and number of 
the corpuscles, that for such purposes it is usual to employ more 
delicate technique according to the object sought by the physician. 






4t 








Fig. 154. — Thoma-Zeiss blood-counting apparatus. A heavy glass slide (a), in the middle of 
which is a cell (B) exactly ^l x millimeter in depth. The cell is limited at the periphery by a 
circular gutter to prevent fluid placed upon the cell from flowing beyond it between the slip 
and cover-glass. The floor of the cell is ruled into squares whose sides are V20 mm - Dark 
lines mark out large squares containing twenty-five small squares. Thick, carefully ground 
cover-glasses (D) are provided in the case. The ordinary Potain Melangeur (S) is used to 
measure and mix the blood. It consists of a capillary tube the upper portion of which is 
blown into a chamber (E) holding 100 c. mm. The stem of the tube is graduated at 0.5 and 
1 c mm. 

Red Blood Cell Counting. — If he wishes to know the number of the 
red cells, he resorts to what is called a hematocytometer, of which the 
best is that called the Thoma-Zeiss apparatus. This is composed of 
two parts. One part is a glass capillary tube, about 10 cm. long, 
with an expansion near the middle, which contains a small movable 
glass ball. On the tube are three marks. Part way up it is marked 



RED BLOOD CELL COUNTING 



0.5, just below the expansion 1, and above the expansion 101. The 
second piece of apparatus is a heavy glass slide, upon which is 
cemented a square of glass with a central circular opening. In the 
centre of this opening is a small disk of glass, which is not as thick as 
that forming the surrounding square, and the surface of which is 
ruled in 400 minute squares, every fifth one being marked by an 
extra line (Fig. 155). If the special cover-glass is now placed over 
the square, it will not touch the surface of the centre disk, but 
leave the space of 0.1 mm. Looking from above downward there 
is seen a cover-glass, and under it a disk which it does not touch; 
between the disk and the boundary of the circular opening is a 
narrow moat. It is upon the upper surface of the ruled disk that 
the drop of diluted blood, about to be described, is placed. 



° t ii ZTZ ii; ' |y* ^. ° j ; v _-- ..- 



Fig. 155.— Appearance of blood in the Thoma-Zeiss cell. 

The finger or ear having been freshly pricked and the first drop 
wiped off, the blood is drawn up to the mark 0.5 or 1.0 in the capil- 
lary tube, and the tip of the tube is then wiped clean. A 0.6 per 
cent, solution of common salt is drawn up after it, until the tube and 
bulb are filled to the point marked 101. The tip of the tube is now 
wiped dry by means of a clean cloth. By shaking the glass ball in 
the tube the blood and salt solution become well mixed in the pro- 
portion of 1 to 100, or 1 to 200, depending upon whether the blood 
was drawn to the 1.0 or 0.5 mark. After the salt solution in the 
lower part of the capillary tube has been forced out by compressing 
the rubber tube of the pipette, and the blood mixture has reached its 
tip, a drop of this homogeneous fluid is forced out so that it rests on 
the surface of the disk, covering the central third. The cover-glass 
is now allowed to fall upon the drop in such a way that all air is 
excluded, and the drop distributed over the surface of the disk. 
The cell should now be allowed to stand for several minutes to 
allow the corpuscles to settle and become stationary, and care should 
be exercised that the stage is perfectly level, as otherwise the blood 
cells will gravitate to one margin. As we look through the micro- 



378 



THE BLOOD 



scope, we now see a space of 16 squares surrounded by double lines, 
and if to these 16 squares we add the squares over which the heavy 
lines run, we have 36 squares under observation. The corpuscles 
arc now counted in series, following the wavy line shown in Fig. 156, 
so that the same square may not be counted twice. After all the 
cells in this group of 36 squares are counted, 5 other groups of 36 
are counted. The total number of red cells is now divided by 6, to 
find the average in each group of 36 squares. This in turn is divided 
by 36, to determine the number in 1 square, and this number is 
multiplied by 800,000 if the blood has been drawn up to 0.5 in the 
pipette, or 400,000 if it has been drawn up to 1. These figures, 
800,000 or 400,000, are not arbitrary, but are based on the fact 
that each square equals 1 to 4000 of a millimeter, and the blood has 




Fig. 156. 



-Method of counting red cells following the direction indicated, 
to avoid mistakes. 



been diluted 200 times or 100 times. Thus we have the following 
approximate process as an illustration: 

Total corpuscles in 216 squares^ 1296-^6 = 216^36=6X800,000 
= 4,800,000 in a cubic millimeter. 

Or if the blood has been diluted 100 times, then we have the 
following illustration : 

Total corpuscles in 216 squares^ 2592^-6=432-^36= 12 X 
400,000 = 4,800,000 in a cubic millimeter. 

For the beginner the procedure is simplified by using only blocks 
of 16 within the double lines, the latter being regarded simply as 
landmarks to separate the different blocks. 

In making the count, it will be found that some of the corpuscles 
overlap the line of a given square, and may lead to error by being 



WHITE BLOOD (ELL COUNTING 379 

counted twice or left out altogether. For this reason it is customary 
to include those corpuscles which overlap the upper and left-hand 
borders. Further, it is best to put down the number of cells found 
in each square as they are counted, and not to attempt to carry the 
addition in the memory, since the loss of one corpuscle makes con- 
siderable difference in the ultimate result. The more squares in- 
cluded in the original count the more accurate the result. 

Immediately after using the apparatus the glass slide should be 
washed in pure water, not alcohol, and the pipette washed out first 
with distilled water and then with alcohol and finally with ether. 

White Blood Cell Counting. — When making the count of the red 
blood corpuscles care should also be taken to estimate the white 
corpuscles, since the proportion of white to red cells often gives us 
very valuable information in disease. This may be done in the 
same specimen by using as a diluent for the blood in the pipette 
what is called Toisson's solution instead of the solution of sail 
already named. This stains the white cells blue, and thus makes 
their counting possible. Toisson's solution is composed of: 

Methyl violet 0.03 (^ grain) 

Neutral glycerin 30.0 (1 ounce) 

Distilled water 80.0 (2>£ ounces) 

Mix thoroughly and add 

Chloride of sodium 1.0 (15 grains] 

Sulphate of sodium 8.0 (2 drachms) 

Distilled water 80.0 [2% ounces) 

As the red cells are counted the number of the white cells can also 
be noted in the 400 squares of the field. By counting several fields, 
made possible in one specimen by the extra rulings of modern 
counting chambers, and taking the average of each the true ratio is 
obtained. Thus if the average is 8 in a dilution of 1 to 100, add three 
ciphers, and 8000 is the number of white cells present. 

When we desire to count the white corpuscles alone, we employ 
a pipette (sometimes called the "white pipette"), which makes the 
dilution of the blood in the proportion of 1 to 10, and we use in place 
of salt solution as a diluent a 0.3 to 1 per cent, solution of glacial 
acetic acid in water. This acid solution dissolves the red corpuscles, 
but makes the white ones more readily seen. The method of cal- 
culating the number of white corpuscles in a cubic millimeter is the 
same as that given for the red corpuscles, except that as the dilution 
is 1 to 10, instead of 1 to 100, we multiply bv 40,000 instead of 
400,000. 

When the large white pipette is used, it will be found that the blood 
is sucked into it much more readily than into the "red pipette," 
because the caliber of this tube is larger. Greater care must there- 



380 



THE BLOOD 



fore be used that the blood or fluid does not quickly pass up above 
the marks on its surface. This fact also causes the blood and fluid 
to run out of the tube very easily if it is held vertically. For this 
reason the bottle holding the diluting fluid should be tipped a little, 
so as to keep the tube as nearly level as possible. Because of the 
large caliber, a greater amount of blood is needed than is usually 
required for blood examination, and, therefore, the puncture of the 
skin must be large enough to permit a free flow. 




157.— Centrifuge. 



Several fields of white cells should be counted, because the number 
of white cells found in a single field are too few to enable us to get 
accurate results, for a variation of one or two cells may make a great 
difference when they are multiplied by so large a figure. This is 
the reason that we do not use the red-cell diluting pipette for this 
purpose. At least 100 white cells should be counted, to obtain 
correct results. The number of leukocytes per cubic millimeter of 
normal blood is from 6000 to 10,000, with a mean of about 7500. 



THE HEMATOCRIT 



381 



The Hematocrit.— A method of obtaining an approximate esti- 
mate of the number of the red and white blood cells is by the 

use of the centrifuge, with the hematocrit attachment (Figs. 157 
and L58 . 

This instrument is used for the volumetric estimation of the rv(\ 
and white blood corpuscles without previous dilution of the blood. 
The hematocrit attachment consists of a metallic frame, carrying 
two graduated capillary glass tubes, 50 mm. long and \ mm. bore, in 
which is placed the freshly drawn blood. These accurately gradu- 
ated glass tubes, seated in rubber-cushioned cups at 1 and 2, are 
held in position securely by spring cups, A A, so that then- is no 




i 



Fig. 158. — Hematocrit attachment for centrifuge. 

possible danger of losing the tubes during rotation. By drawing 
back the milled heads, H II, the tubes are instantly released and 
as quickly clamped again into position Fig. 158). This apparatus 
should be made of aluminum, in order that it be strong and light. 
The advantage gained by the use of tin- metal i- that it is possible 
to greatly increase the length of the arms of the hematocrit, thereby 
taking advantage of the well-known law of mechanics that "the 
centrifugal forces of two equal bodies, moving with equal velocity 
at different distances from the centre, are inversely as their distance 
from the centre." In order, therefore, to obtain any desired amount 



Fig. 159 



of centrifugal force it is not necessary to increase the speed of the 
machine, but simply to increase the distance from the centre. 

The finger of the patient is thoroughly cleansed with water, and 
then punctured by means of a spear-pointed needle. The first drop 
of blood is rejected, and a second drop is secured by very slight 
pressure. The blood is then drawn, by suction, by means of a con- 
stricted dropper (Fig. 159), with rubber-bulb connection, into the 
capillary tube, which is then placed in the hematocrit and rapidly 
revolved for at least one minute. 

The rapidity and simplicity of this process are theoretically at 
once apparent. The blood does not have time to coagulate, and 



3S2 THE BLOOD 

by the centrifugal force the red corpuscles, having the greatest 
specific gravity, are thrown to the distal extremity of the tube, and 
will occupy about one-half of the tube, or to the mark 50. 

The white corpuscles, next in specific gravity, will occupy a posi- 
tion between the red corpuscles and the liquor sanguinis, which is 
found in the proximal end of the tube, quite clear and free from 
corpuscles. 

When the column of red blood corpuscles extends to mark. 50 we 
have, as a rule, about 5,000,000 red corpuscles per cubic milli- 
meter; but if the precipitated corpuscles reach only mark 30, 
there are only about 3,000,000 per cubic millimeter, or 60 volume 
per cent. If they reach only mark 20, there are about 2,000,000 
per cubic millimeter, or 40 volume per cent. 

This method of blood estimation was highly thought of when 
first introduced; it later largely lost its popularity, but now is again 
receiving some attention. For determining the number of red cells 
it must always be subject to grave error because of the change in 
size of these cells in many conditions. It furnishes valuable infor- 
mation regarding the total volume of the red cells. 

Significance of Variations in Number of the Red Cells. — Changes in 
number of the red cells are of practical diagnostic importance. 
They are diminished, oligocythemia, in essentially all cases of 
anemia of whatever type, though in some this reduction does 
not form the most striking feature of the blood condition. The 
decrease is especially prominent in the secondary anemia of certain 
infections and parasitic diseases and in pernicious anemia. An 
increased number of red cells, polycythemia, is constant in the new- 
born and often attains an extraordinary degree in cases of congenital 
heart disease, in persons who remove from lower to higher altitudes, 
and in the subjects of that little-understood affection characterized 
also by chronic cyanosis and enlarged spleen, chronic polycythemia 
with splenomegaly. In the last-named condition counts as high as 
12,000,000 have been recorded. 

(For a discussion of the Blood Diseases, see the latter part of this 
chapter.) 

Differentiation of the Leukocytes.— Continuing the examination 
of the blood for definite diagnostic purposes, we find that a very 
important part of this study consists in the differentiation of the 
various forms of white blood cells. These cells appear in the blood 
of healthy individuals in five forms : 

1. They occur as white cells the size of, or smaller or larger than, 
the ordinary red cell. Each of these small white cells contains a 
nucleus so large that it almost completely fills the body of the cell, 
the protoplasm being a narrow rim or not discernible. They are 
called lymphocytes and form about 20 per cent, of the total number 



DIFFERENTIATION OF Till-: LEUKOCYTES 383 

of while cells in health. They are not phagocytic, nor actively 

ameboid. 

2. They occur as what are called large mononuclear leukocytes, 
or hyaline cells, or large lymphocytes, much larger than the red cells, 
possessing a moderately large single nucleus, which is surrounded 
by a zone of pale non-granular protoplasm. Sometimes these cells 
show a change in the shape of the nucleus, and are then called 
transitional leukocytes. These mononuclear cells make about 
5 to 8 per cent, of the white blood cells. 

3. They occur as large white cells with a nucleus of irregular 
shape (polymorphous nucleus), or a nucleus split up into several 
smaller nuclei (polynuclear). They are often for this reason called 
polymorphonuclear or polynuclear leukocytes. Their protoplasm 
contains fine granules, which stain when brought in contact with 
neutral dyes, and for this reason these cells are often called neutro- 
philes. A neutrophile, a polymorphous leukocyte, and a polynuclear 
leukocyte are, therefore, one and the same thing. They equal about 
70 per cent, of the white blood cells and are actively ameboid and 
phagocytic. 

4. Polymorphonuclear cells, usually slightly smaller than the 
preceding, containing very coarse granules, w r hich stain when brought 
in contact with acid dyes, of which the chief is eosin. They are 
called eosinophils, and are limited in number to 2 or 3 per cent. 
These cells possess ameboid movement, but are not phagocytes. 

5. Basophile cells. In size and in shape of nucleus they resemble 
the polymorphonuclear leukocyte, but the protoplasm contains 
basic-staining granules, variable in size. They are not above 0.5 
per cent, in normal blood. 

In disease we find variations from these types as to proportional 
and actual number, and in addition- other white cells are present. 
The most important abnormal leukocyte is the myelocyte or marrow 
cell, never found in normal blood. It is a round or oval cell, often 
larger than the large mononuclear which it resembles except that 
the protoplasm contains acid, neutral, or basic-staining granules. 
The neutral or neutrophile type is the one most frequently found. 

In order that the various forms of white cells that we have named 
may be readily separated from one another we have to resort to cer- 
tain stains, it having been shown by Ehrlich and many others that 
the nuclei of these cells are susceptible to different stains, as are also 
the granules found in their protoplasm. These stains differ as to 
their color and reaction. We have basic stains and acid stains, but 
these terms are largely arbitrary and it is not to be thought that they 
are actually acid or basic in their chemical reactions. As a rule, 
the acid stains affect the protoplasm of a cell, and the basic stains 
the nuclei. The basic stains are methylene blue, methvl violet, 



384 THE BLOOD 

methyl green, hematoxylin, and gentian violet. The acid stains 
are picric acid, eosin, orange G, and acid fuchsin. The cells whose 
protoplasmic granules stain with basic stains are sometimes called 
basophiles, those whose protoplasm is stained by acid stains acido- 
phils (eosinophiles), and those cells which stain with both acid and 
basic stains neutrophiles. Further, these stains render the nucleus 
one color and the granules another, as in Plate XI, in several of 
the figures of which will be found cells with red granules and blue 
nuclei. 

One of the best solutions for staining purposes is that of Ehrlich, 
which is called a triple stain. It is composed as follows: saturated 
watery solution of orange G, 6 c.c; saturated hydro-alcoholic (20 
cent, of alcohol) solution of acid fuchsin, 4 c.c. These ingredients 
having been mixed gradually and thoroughly shaken, the following 
constituents are added, the shaking being continued : saturated watery 
solution of methyl green, 6.6 c.c; absolute alcohol, 10 c.c; glycerin, 
5 c.c; water, 5 c.c This solution should stand for twenty-four 
hours, to allow of sedimentation; it improves with age; and when it 
is used the supernatant liquid is to be drawn off by a pipette in order 
to avoid the sediment. It must not be filtered. This stain acts in 
a few minutes. 

Cover-glass films, made as already described, are heated over an 
alcohol flame or on a hot stage made of sheet copper or in an oven, 
and kept at 120° to 140° C. for fifteen minutes to half an hour. 
After this they are placed in the staining fluid for from one to four 
minutes, then washed in pure water, dried, and mounted in Canada 
balsam or cedar oil. The Canada balsam should not be prepared 
with chloroform, as it will decolorize the specimen. The film is 
then ready for microscopic examination with a one-twelfth oil- 
immersion lens. The eosinophile granules in the corpuscles will 
be stained a reddish hue, the neutrophile granules lavender or purple, 
and the nuclei bluish green or blue. The greatest objection to this 
stain is that it does not stain basophile granules nor parasites. 
(See Plate XI.) 

For routine blood work Ehrlich's stain is being largely superseded 
by the various polychrome methylene blue-eosin combinations, of 
which those bearing the names of Leishman, Wright, and Hastings 
are well known. These stains possess several advantages. Films 
need no previous fixation (the menstruum being pure methyl alcohol) 
and basophile granules and parasites are well stained. Neutro- 
phile granules, however, are usually not so well stained as by Ehrlich's 
method. All these stains are made after complex formulas which 
need not here be given, as the practitioner had best obtain them 
already prepared. The technique for using them all is very similar. 
The dried, unfixed film is covered by a few drops of the stain to 



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PLATE XI. 

BLOOD. 

( Ehrlich triple stain.) 
(Prepared by I)n. I. P. Lyon.) 

Fig. I. TYPES OF LEUCOCYTES. 

a. Polymorphonuclear Neutrophile. b. Polymorphonuclear Eosinophile. c. Myelocyte 
(Neutrophilic), d. Eosinophilic Myelocyte, e. Large Lymphocyte (large Mononuclear). 
/. Small Lymphocyte (small Mononuclear). 

Fig. II. NORMAL BLOOD. 
Field contains one neutrophil. Reds are normal. 

Fig. III. ANiCMIA, POST-OPERATIVE (secondary). 

The reds are fewer than normal, and are deficient in haemoglobin and somewhat 
rregular in form. One normoblast is seen in the field, and two neutrophiles and one 
small lymphocyte, showing a marked post-hsemorrhagic anaemia, with leucocytosis. 

Fig. IV. LEUCOCYTOSIS, INFLAMMATORY. 

The reds are normal. A marked leucocytosis is shown, with five neutrophiles and 
one small lymphocyte. This illustration may also serve the purpose of showing the 
leucocytosis of malignant tumor. 

Fig. V. TRICHINOSIS. 
A marked leucocytosis is shown, consisting of an eosinophilia. 

Fig. VI. LYMPHATIC LEUKEMIA. 

Slight anaemia. A large relative and absolute increase of the lymphocytes (chiefly 
the small lymphocytes) is shown. 

Fig. VII. SPLENO-MYELOGENOUS LEUKAEMIA. 

The reds show a secondary anaemia. Two normoblasts are shown. The leucocytosis 
is massive. Twenty leucocytes are shown, consisting of nine neutrophiles, seven myelo- 
sytes, two small lymphocytes, one eosinophile (polymorphonuclear) and one eosinophilic 
myelocyte. Note the polymorphous condition of the leucocytes, i.e., their variations 
from the typical in size and form. 



Fig. VIII. VARIETIES OF RED CORPUSCLES. 

a. Normal Red Corpuscle (normocyte), b, c. Anaemic Red Corpuscles, d-g. Poikilocytes. 
h. Mierocyte. i. Megaloeyte. j-n. Nucleated Red Corpuscles. j,k. Normoblasts. I. Micro- 
blast. m,n. Megaloblasts. 



ESTIMATION OF HEMOGLOBIN 385 

which, after the lapse of one minute, is added drop by drop distilled 
water until a scum forms or until a predetermined amount has been 
added, it being necessary experimentally to determine the exact 
quantity for each lot of the stain. The diluted stain is allowed to 
act for three or four minutes, washed off with water, the film blotted 
dry and mounted in balsam. Nuclei are stained blue or lilac, neutro- 
phil and eosinophil granules pink, basophile granules blue or 
purple, the protoplasm of the lymphocyte a deeper, of the large 
mononuclear a paler, blue than the nucleus. 

Changes in form, size, and staining reaction of the red cells are 
determined by the examination of stained films made in the follow- 
ing manner: The centre of a clean cover-glass is touched to a 
small drop of freshly drawn blood and immediately dropped, blood 
side downward, upon a second cover. The instant the blood ceases 
spreading, the two covers should be rapidly drawn apart, without 
pressure or lifting, and the films allowed to dry in the air. They 
are then stained by one of the methods described in connection with 
the leukocytes. The properly made film is made up, except at the 
periphery, of a single layer of red cells. 

Massive changes in staining reaction, polvehromatophilia, and 
punctate basic areas, granular or basophilic degeneration, may 
in this way be detected. Basophilia is an almost constant feature 
in chronic lead poisoning. 

In the anemias are found deformed red cells known as poikilocytes. 
Small red cells, microcytes, and large cells, macrocytes or megalo- 
cytes, may also be present; the former are occasionally found in nor- 
mal blood. Nucleated erythrocytes, microblasts, normoblasts, or 
megaloblasts, according to their size, appear under certain circum- 
stances. Cells may contain vacuoles or be so deficient in hemoglobin 
as properly to be called "shadow corpuscles." Some of the diseases 
in which these changes are found will be discussed farther on. 

Estimation of Hemoglobin. — Having discovered the number and 
the quality of the red corpuscles, an equally important measure 
is to determine the quantity of hemoglobin which they contain. 
This is often done by the use of the hemoglobinometer of von 
Fleischl, although that of Gowers is sometimes used. Fleischl's 
apparatus consists of a small table, in the centre of which is a 
hole into which fits a cylindric chamber with a glass bottom, 
divided perpendicularly in the middle by a metal diaphragm, the 
space on one side of which is filled with pure water, that on the 
other with diluted blood. Under the stand is a frame in which 
is set a piece of colored glass as near the hue of diluted blood as 
possible, and tapered off gradually, so as to give a lighter shade 
of red at one end than at the other. The frame carrying this glass 
25 



386 



THE BLOOD 



wedge is marked by a graduated scale, and is moved from side to 
sidewinder the half of the cylinder, which is to contain only pure 
water, by a thumb screw. Beneath the glass and cylinder is a white 
reflector" to direct the rays of light through them (Fig. 160). The 
rest of the apparatus consists in a little capillary tube attached to a 
tiny metal handle. This tube will hold just enough pure and healthy 
blood to color the water on one side of the cylinder to the hue shown 
in the colored glass when it is opposite the normal mark "100." 
The finger being punctured, the end of the capillary tube is lightly 
touched to the drop of blood, which fills the tube. The blood is 




Fig. 160. — Von Fleischl's hemoglobinometei\ 

now washed from the capillary tube into one of the sections of the 
hemometer container, into which was previously placed a few drops 
of water, by directing through the tube a stream of distilled water 
from a fine-pointed pipette. After thoroughly mixing the blood and 
water with the handle of the pipette, both compartments are filled 
to the brim with distilled water. The inside of the capillary tube 
should be perfectly dry before filling it with blood, and, when filled, 
no blood should be allowed to cling to the outside. Neglect of these 
precautions invites serious inaccuracies in the results obtained. The 
apparatus is then exposed to candle- or lamplight, because with day- 



ESTIMATION OF HEMOGLOBIN ;;s; 

light the hue of the glass docs not match Mood color, and the frame 
[s moved under the side of the cylinder, which contains only pure 
water, until the glass seems to the eve to match the fluid containing 
the blood on the side through which the pure light streams. If 
the glass matches the blood color when the mark on the frame is at 
50, it shows that the hemoglobin equals only 50 per cent, of normal; 
or if it is at 85, it signifies 85 per cent. As a matter of fact, an exami- 
nation of perfectly healthy blood will often give not more than 85 
to 90 per cent, of hemoglobin with this apparatus. 

Care should be taken in regard to three points: first, to be sure 
that all the blood is washed out of the capillary tube into the water; 
second, that the two halves of the cylinder are filled to the brim with 
water, so that there is neither a positive nor a negative meniscus; 
third, to be careful to cleanse the entire apparatus thoroughly after 
each use of it before putting it away. 

A ^ R 

r 




Fig. 161.— Dare's hemoglobinometer. W. Blood holder. R. Wheel to turn color gla—. 
l. Color glass. 1. Observation tube. T. Shade. 1'. Candle. 

Miescher has recently modified the apparatus of von Fleischl in 
a way that ensures greater accuracy, but the instrument is so com- 
plex as to be practicable only for laboratory use. It possesses the 
very desirable feature of giving the hemoglobin reading in grams per 
100 c.c. of blood instead of in per cent., as do other instruments. 

A better apparatus than that of von Fleischl has recently been 
introduced by Dr. Arthur Dare, formerly one of the assistants in 
my clinic at the Jefferson Medical College Hospital. It may be 
described as follows : 

The application of this instrument depends upon the principle 
that the color of a thin film of undiluted blood, illuminated by 
candle-light, may be compared with a graduated color comparison. 
It has the advantage over other methods employed for a similar 
purpose, that while but a small drop of fluid is needed for its 



388 THE BLOOD 

application, this consists of pure blood undiluted with artificial 
serums. 

The technique and possible errors of dilution are thereby entirely 
eliminated, and leukocytosis, which is a frequent source of error in 
hemoglobin estimations, imparting as it does a turbidity to mixtures 
of blood and water, becomes imperceptible when viewed by trans- 
mitted light against an opaque background, the red color of the 
hemoglobin only becoming visible, while the opacity due to increase 
in the number of leukocytes is incalculable. 

Furthermore, the shades of color to be compared are very decided, 
even in blood markedly deficient in hemoglobin, and thus facilitates 
accurate comparison. Besides the colorimetric principle, there is 
an element of density, due to concentration of Coloring matter present 
in the blood film, that magnifies the shade of color, giving a wider 
range between decimal points, ensuring more uniform comparison 
and greatly reducing the "personal equation" of estimation exist- 
ing in different individuals. 

The examination, which consists of collecting the blood and the 
estimation of hemoglobin percentage by comparison with the gradu- 
ated color scale, requires very little time for its accomplishment. 
The plane surfaces of the blood pipette are quickly cleansed and 
the whole procedure completed in a very brief period. 

Still another method of estimating the hemoglobin, which does 
not require any costly apparatus, but for which considerable tech- 
nical skill is necessary, is the so-called specific gravity method. This 
is Hammerschlag's modification of Roy's method. Chloroform and 
benzol are mixed in an ordinary urinometer tube, so that their specific 
gravity is 1059 — in other words, that of normal blood. A drop 
of blood obtained by the ordinary method of puncture is dropped 
into this mixture in such a way that it does not touch the sides 
of the urinometer tube. The drop floats undissolved in the chloro- 
form and benzol mixture. If it sinks to the bottom, its specific 
gravity is higher than normal, and we add a few drops of the heavier 
ingredient, chloroform, until the blood drop floats free in the mixture. 
If, on the other hand, it rises, we add the lighter benzol until it 
becomes suspended. The specific gravity of the fluid, which must be 
also that of the blood, is now taken, and if it is above normal we 
have reason to believe that the hemoglobin is above normal, or if it 
is below normal, that the hemoglobin is scanty. This is true in 
persons in ordinary disease, but in dropsy, when the red cells may 
be water-soaked and heavy, or in leukemia, when the white cells are 
present in excess, the specific gravity may be excessive and yet the 
hemoglobin below normal. Otherwise the test is fairly accurate, 
since the specific gravity of the blood cells depends largely on their 
content of hemoglobin. The various specific gravities equal the 



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COLOR INDEX 

percentage of hemoglobin in the following proportion-, according 
Hammerschlag: 

1033 to 1035 = 25 to 30 per cent. 1048 to 10ft " i>er cent. 

5 to 1038 = 30 to 35 1080 to 1053 = 65 to 70 " 

1038 to 1010 35 to 40 " " 'to 1055 =70 to 

1040 to 1046 40 to IS • " ".to 1057 = 75 to 85 " 

1045 to 1048 4o to 55 " " 1057 to 1060 = 85 to 95 u 

Another method, not so accurate but useful in lieu of those de- 
scribed, for estimating the hemoglobin, has been devised by Tall- 
quist, and consists in taking up a drop of blood with pure white 
bibulous paper and promptly comparing the saturated area with 
a correct hemoglobin color scale. The test should be made in 
direct sunlight. This is, of course, a very simple and only 
approximately correct method. Sec Plate XII. 

Estimation of the hemoglobin is one of the most valuable points 
in a blood examination. A fairly high hemoglobin content may l>e 
found in the blood of persons presenting the superficial appearances 
of well-marked anemia and conversely a low amount in the appar- 
ently healthy. The normal amount i- regarded as 1<><) per cent., 
but often the reading is below this, to 95 or in females even 90, in 
persons with perfect health. 

Reduction in hemoglobin, oUgochromemia, occurs in all type- of 
anemia, but is absolutely and also relatively to the red cells much 
more severe in some than in others. I>a Costa finds these average 
readings: In pernicious anemia, 25 per cent.; in leukemia. 39 per 
cent.; chlorosis, 43 per cent. ; secondary anemia, 55 per cent. An 
increased hemoglobin percentage may be present during temporary 
concentration of the blood and commonly accompanies polycythemia, 
in some types of which it has been found to reach 2(><) per cent. 

In important cases the several methods of estimating hemoglobin 
should be used before a definite decision as to the exact percentage 
is reached. 

Color Index. — Not only is it desirable to estimate the quantity 
of hemoglobin which may be present in the blood, but also to 
know the relative richness of hemoglobin in each corpuscle. 
Thus, in chlorosis the red cells may be nearly normal in num- 
ber but sadly lacking in hemoglobin. In pernicious anemia 
the reverse condition is present. To determine this, we divide 
the percentage of hemoglobin by the percentage of red cells. For 
example, suppose we find that the hemoglobin is present in the 
normal amount of 100 per cent., and a blood count reveals in 
a man 5,000,000 corpuscles to a cubic millimeter, we know that 
the percentage of red cells is also 100. We, therefore, divide 100 
per cent, of hemoglobin into 100 per cent, of red cells, and 1 
is the result. This is said to be the color index, and indicates 



390 THE BLOOD 

that each cell is normally rich in coloring matter. The color index 
may, however, be apparently normal, and yet anemia be present, 
for if the red cells be reduced to 2,500,000, or 50 per cent., and the 
hemoglobin to 50 per cent., or one-half, the index would still be 1. 
In chlorosis, however, the cells might be 4,000,000, or 80 per cent., 
and the hemoglobin 50 per cent., in which case we follow the rule 
to divide the percentage of hemoglobin by the percentage of red 
cells, which would be 50 -r- 80 = 0.6 + , or if in pernicious anemia 
the red cells are 1,000,000, or 20 per cent., and the hemoglobin is 
40 per cent., we find that 40 h- 20 = 2. Each cell here contains twice 
its normal amount of hemoglobin, yet there is actually a great lack 
of it in the blood as a whole. 



DISEASES IN WHICH THE CHIEF CHANGES ARE IN THE 

RED CELLS. 

Anemia. — Having studied the methods of examining the blood, 
we come next to the consideration of the diagnostic value of the con- 
ditions which we find in it. We find, first, that anemia, or blood 
deficiency, is represented by two conditions, in one of which the 
pallor and other symptoms are due to a diminution in the number of 
red blood corpuscles, while in the other there is a decrease in the 
amount of hemoglobin in each corpuscle. In regard to the white 
corpuscles we find even more valuable diagnostic data, since their 
variation in number, form, and character is marked in some diseases. 
Practically all conditions of the blood which are pathological repre- 
sent diseases in organs connected with the blood directly or indirectly, 
and do not depend upon primary changes in this liquid, except in 
rare instances. 

Secondary Anemia. — A patient's blood having been found lacking 
in the proper number of red blood corpuscles, the question naturally 
arises as to what conditions underlie this variation from the normal. 
The most common causes of this decrease are the infectious diseases, 
all of which result in producing a degree of anemia most marked 
during early convalescence; the history of such an attack should 
always be sought, and, if found, regarded as an important point for 
consideration in reaching a diagnosis. If there be no history of 
acute illness, the most natural condition to be thought of is that 
known as simple anemia, produced by no apparent disease of the 
organs of the body, but due to lack of good food, pure air, proper 
hygienic surroundings, and exercise. If this be excluded from the 
diagnosis, we must not forget that if food is taken and not 
absorbed properly the corpuscular richness of the blood is de- 
creased, and, therefore, chronic indigestion may be the cause of the 



DISEASES IN WHICH run CHANGES are IN RED CELLS 39] 



rli 



fficulty. Again, profound anemia, as to the number of the rod 
blood corpuscles, may be present and seem inexplicable, until it is 
discovered that the patient suffers from bleeding hemorrhoids, and 
the daily loss of blood, even though it be small, is sufficient to 
produce anemia. Similarly repeated attacks of wise-bleed or of 
excessive menstruation may so result. Naturally the physician 
will have excluded the possibility of the anemia being due to a 
single profuse hemorrhage from any cause before searching as far 
as this for a diagnosis. 

In addition to these causes of anemia we find anemia due to a 
decrease in both the corpuscles and hemoglobin. A large proportion 
of these cases have already been mentioned when speaking of the 
anemias of convalescence and hemorrhage, but a far more important 
cause of this condition, yet one often overlooked, to the great regret 
of the physician in later years, is tuberculosis. Still other causes 
of such anemia are sarcoma, renal disease, and cancer, particularly 
gastric cancer, in which condition the blood may resemble that of 
pernicious anemia, and gastric ulcer, in which the loss of corpuscles 
may also be extraordinary, even if no hemorrhage occurs. Chronic 
lead poisoning, arsenical poisoning, and uremic poisoning may 
cause it, and it arises from the presence of numerous forms of intes- 
tinal parasites, such as tape-worm and Ankylostcmum duodenale 
or Uncinaria arnericana, and last, but by no means least, from 
malarial infection, either as manifested by acute attacks, frequently 
repeated, or by slow poisoning, with the development of cachexia. 
(See farther on in this chapter.) 

In the foregoing group of anemias, broadly classed as secondary 
anemias because the blood condition is clearly a sequence of some 
recognizable affection primary in other tissues, the blood picture is 
in general as follows: The hemoglobin is diminished, usually more 
than are the erythrocytes, hence the color index is lowered. The 
red cells are moderately reduced in numbers except in extreme cases. 
Poikilocytes and erythroblasts are present in severe cases, the latter 
being normoblasts or possibly microblasts in type. The leukocytes a re 
commonly increased, a quite well-defined polvnuclear leukocytosis 
being the rule. Myelocytes in very small numbers may be present. 

Estimations of hemoglobin and red cells are of value in certain 
acute conditions. If a patient is brought to the physician in a state 
of advanced anemia, acute or chronic, and needs an operative pro- 
cedure for relief, and the hemoglobin is below 3.3 per cent., it is 
well to remember the rule of Mikulicz, which is, "Do not operate." 

Again, a great decrease in hemoglobin and red cells would aid in 
separating the collapse of concealed hemorrhage, as in a case of 
rupture of the tube in extra-uterine pregnancy, from other conditions 
of collapse not dependent on loss of blood. 



392 THE BLOOD 

Primary Anemias. — There still remains to be considered the 
primary anemias, of which one is called pernicious, in that it pro- 
gressively gets worse until death occurs in the majority of cases. 
At present we do not understand the pathogenesis of this disease. 
It is characterized by marked pallor without loss of flesh, or, to speak 
more correctly, the subcutaneous tissues are added to rather than 
robbed of fat. There are gradually increasing dyspnea, failure of 
strength, cardiac palpitation, venous murmurs, some vertigo, and 
roaring in the ears. The blood shows a most extraordinary and con- 
tinually diminishing number of red blood corpuscles, the count in 
one recorded case being only 143,000 to the cubic millimeter. In 
addition, the following points of great diagnostic importance are to 
be noted: First, the individual red corpuscles are richer than 
normal in hemoglobin, the color index often being above normal; 
second, many of them are larger than normal (megalocytes), pro- 
ducing a high volume index; third, the red corpuscles are deformed, 
some being ovoid, others irregular in shape from projections and 
constrictions on their surfaces (poikilocytes) ; fourth, there are present 
microcytes, or red blood cells which are smaller than normal; fifth, 
nucleated red blood cells, quite constantly large cells named mega- 
loblasts, which have a pale staining nucleus. These last are often 
larger than the megalocytes, and are sometimes called the "cor- 
puscles of Ehrlich," since he regards them as pathognomonic of 
pernicious anemia. Normoblasts also may be present. The white 
blood corpuscles are normal in number, or decreased, with a rela- 
tive increase of lymphocytes and possibly a few myelocytes, 
although the great diminution in the red cells renders the proportion 
of white to red greater than normal. Cases of pernicious anemia 
in which there are no regenerative changes in the bone-marrow 
are known as aplastic anemia. This type is rapidly fatal, the chief 
differences in the blood picture from that described being a low 
color index and the absence of megaloblasts. 

Another form of anemia, which at one time was considered 
secondary but now classed as primary, is called chlorosis. In this 
state the corpuscular diminution is so slight that it maybe ignored; 
but the decrease in hemoglobin is extraordinary, sometimes falling as 
low as 30 per cent, of the normal or below it, the color index often 
being as low as 0.5. The red corpuscles are, however, in severe cases 
irregular in form — that is, there is more or less poikilocytosis, and 
many of them may be undersized. The white corpuscles remain 
normal in number or are slightly increased. Normoblasts are occa- 
sionally found in chlorosis of a severe type, but the larger varieties of 
nucleated erythrocytes are seldom seen. The diagnostic points of 
chlorosis, in addition to those just named, are the facts that the patient 
is generally a girl of from fourteen to twenty-five years, that the skin 



DISEASES IN WHICH THE CHANGES ARE IN WHITE CELLS 393 

is peculiar in its pallor (see chapter on the Skin), and that there is 
often little if any menstrual How, which is usually only faintly pink 
in hue. Dyspnea, cardiac irregularity, constipation, and a wayward 
appetite are often present. Auscultation of the neck on the right 
side over the jugular vein will reveal a peculiar murmur called a 
" humming-top" murmur. Febrile movement of slight degree may 
also he present. 

Polycythemia. — Polycythemia, or that state in which there at 
least appears to be an actual increase in the number of ed cells to 
an abnormally high degree, is met with in instances in which there 
is concentration of the blood by diarrhea or excessive diuresis. An 
actual or real polycythemia is also met with in certain cases of 
congenital heart disease, in those who live at high altitudes, and in 
cases of tracheal stenosis. The most interesting ot all the instances 
of polycythemia is that called chronic splenomegalic polycythemia 
which is characterized by an increase of the red cells to as high a 
number as 7,500,000 or more and progressive asthenia, high arterial 
tension, cyanosis, and enlargement of the spleen. The white cells 
are not increased. 



DISEASES IN WHICH THE CHIEF CHANGES ARE IN THE 
WHITE CELLS. 

There yet remains to be considered those conditions in which we 
find not only some of the states already described, but, in addition, 
marked alterations in the white blood corpuscles as well as the red, 
alterations of such moment that they become the salient features of 
the blood when it is examined. These are of great diagnostic 
importance. 

The points of importance in examining blood in regard to the 
white corpuscles are their number and their peculiarities and kinds. 
Before doing so, however, it must be borne in mind that the pro- 
portion of white cells in different individuals varies very greatly in 
the limits of health, being increased by the taking of food ^digestion 
leukocytosis), by pregnancy (gravid leukocytosis), by violent exer- 
cise, and by massage. Starvation correspondingly decreases the 
white cells. Digestion leukoevtosis usually lasts for two to four 
hours after a meal. In these changes the relative percentage of 
all forms of white cells except the eosinophils may be increased, 
although in most cases the polymorphonuclear cells are in excess. 
Again, much depends upon the general state of the patient's health 
and nutrition. A shrivelled, old woman may have as low a propor- 
tion as 40 per cent., and a stalwart, athletic man have SO per cent, of 
polynuclear leukocytes, and be in perfect health. Usually, it may 



394 



THE BLOOD 



be considered that about 60 per cent, of these polymorphonuclear 
cells is normal, but the individual characteristics must be taken into 
account in determining the diagnostic value of the percentage. 

Leukemia. — When the disease splenomedullary leukemia is present, 
the total leukocyte count usually ranges between 200,000 and 500,000 
per cubic millimeter, though very much higher figures have been 
attained. The typical change in the blood is the presence of the 
so-called myelocyte of Ehrlich, the abnormal leukocyte previously 
described. This often forms 20 per cent, or more of the leukocytes. 




Fig. 162. 



Splenomedullary leukemia, showing outline of enormous spleen in a boy 
of fourteen years. (Author's wards.) 



Mast-cells are also a conspicuous feature. The ordinary large 
mononuclear cells are not greatly increased, and the polymorphous 
or polynuclear cells are decreased relatively though absolutely in- 
creased. Eosinophile cells are often both absolutely and relatively 
increased, though they may not be present. At one time they were 
supposed to be pathognomonic of this disease, but they are not so 
considered at this time. 

The other changes found in leukemia are that the red blood 
cells are decreased in number, and a large number of nucleated 
forms, chiefly normoblasts, may be seen. The hemoglobin is also 



DISEASES IN WHICH THE CHANGES ARE IN WHITE ('ELLS 395 

decreased. The symptoms of this form of leukemia are pallor and 
puffiness of the face, dyspnea, and general feebleness, with great 
and gradual enlargement of the spleen and liver, and marked 
splenic tenderness. Auscultation over this organ may reveal a 
murmur and palpation a crepitus. Hemorrhage, generally from 
the nose, is common, and dyspnea and diarrhea are often present. 
Frequently retinitis develops, and slight fever may occur. This is 
by far the more common form of leukemia. 

In advanced anemia, when the proportion of white to red cells 
is 1 to 10, and the lymphocytes (that is, the mononuclear, deeper- 
staining cells, with a rim of non-granular protoplasm), or the large 
mononuclear, are greatly increased in number, we suspect lymphatic 
leukemia. Myelocytes, so typical of the splenomedullary form, 
appear in this condition only in very small numbers if at all and 
splenic enlargement is absent, but in its place there is often enlarge- 
ment of the superficial lymph nodes, though these never grow so 
large as in Hodgkin's disease, or pseudoleukemia. (See chapter 
on Fevers.) The acute form of this disease often presents the clini- 
cal features of a severe acute infection. 

Pseudoleukemia, or Hodgkin's disease, is to be differentiated from 
true leukemia by the blood examination, it being recalled that in this 
malady there is usually only a slight decrease in the red cells and no 
other marked changes. Recently, however, Martin and Matthew- 
son have emphasized the fact that in some cases of pseudoleukemia 
the lymphocytes have increased as greatly as in many instances of 
true lymphatic leukemia. As a general rule, however, the blood 
condition separates the affections. (For Band's 1 )isease, see page .'510.) 

Leukocytosis in Acute Diseases. — We study the white cells as to 
their number and character for other diagnostic purposes than those 
alieady mentioned, namely, for the discovery and differentiation of 
acute infectious diseases. Thus, in nearly all infections associated 
with acute inflammation we find an increase in the white cells, or 
leukocytosis. The particular white cell increased under these circum- 
stances is the polymorphonuclear. Acute croupous pneumonia 
is particularly apt to produce this state unless infection is very 
virulent, when reaction fails to occur. By studying leukocytosis 
we can often decide as to the presence of deep-seated inflam- 
mations. Thus in doubtful cases of appendicitis a study of the 
leukocytes will aid the diagnosis and separate the condition from 
obscure non-inflammatory states. If an increase of the polymorpho- 
nuclear cells is present, we can exclude gallstone colic, renal colic, 
fecal colic, and ovarian neuralgia, unless there is associated with one 
of these affections an acute inflammation. The degree of leukocy- 
tosis in a case of appendicitis in the early stages is in direct ratio to 
the severity of the process. So, too, if leukocytosis gradually in- 



396 THE BLOOD 

creases, it is a sign of spreading inflammation. If it is absent after 
several days' illness with appendicular symptoms, its absence may 
indicate sepsis of a very grave form. It is important to recall in 
this connection the fact that a high leukocyte count is met with very 
early in intestinal obstruction. If it speedily falls, intestinal gan- 
grene is to be suspected. 

Often accompanying inflammatory leukocytosis is the condition 
known as iodophilia, or the presence in the polynuclear leukocytes 
or plasma of iodine-staining granules. This is specially prominent 
when suppurative products are being absorbed but is by no means 
limited to cases of pus formation. 

Leukocytosis is usually absent in typhoid fever, malaria, severe 
septicemia, tuberculosis in all its forms, in influenza, and in measles, 
in many cases there being an actual diminution, leukopenia, in 
the number of white cells. Should some complicating focus of acute 
inflammation be developed, then leukocytosis appears. In suspected 
typhoid fever the absence of leukocytosis, with a diminution of the 
multinuclear cells and an increase in the mononuclear cells, is of 
importance in pointing to the presence of this malady. Should per- 
foration of the intestine ensue, leukocytosis is apt to occur, unless a 
general peritonitis is produced, when the number of leukocytes in 
the peripheral circulation may be decreased by the outpouring of 
cells into the abdominal cavity. 

An increase of the eosinophile cells, or eosinophilia, occurs in 
cases of skin disease and other conditions, but is of special diagnostic 
value in parasitic affections, in particular trichiniasis and ankylo- 
stomiasis. 

A moderate leukocytosis occurs after childbirth, and is normal 
at this time, but does not persist during lactation. 

Toward the end of prolonged fatal illness, or where the onset of 
death is gradual, an increase in white cells develops, called terminal 
leukocytosis. 

PARASITES OF THE BLOOD. 

We still have for consideration the parasitic diseases of the blood. 
Of these the most important are due to the presence of the malarial 
germ of Laveran, or, as it is more properly called, the "hematozoon 
malaria" of Marchiafava and Celli, the Filaria sanguinis hominis, 
and the Trypanosoma. 

Malarial Organisms. — No more important addition to the study 
of disease from a diagnostic standpoint has been made than the dis- 
covery of the presence of a parasite in the blood of persons suffering 
from malarial fever, a parasite which is always present under these 
circumstances, and in all probability acts as the cause of all malarial 











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PARASITES OF THE BLOOD 397 

manifestations. These parasites arc varieties of sporozoa, which 
develop inside the red blood corpuscles of the individual attacked.' 

The parasite of malarial fever occurs in three forms, namely, as 
that of tertian fever, that of quartan fever, and as the parasite of the 
so-called estivo-autumnal fever. 

The Tertian Parasite. — The intracorpuscular tertian parasite first 
appears as a small hyaline, colorless body, which occupies but a 
slight extent of the interior of the red blood corpuscles. (See Plate 
XIII, Figs. 2, 3 and 4. 2 ) When quiet it is round, like the corpuscle 
in which it lies; but if the specimen examined be fresh, it may be 
seen to possess active ameboid movements, thereby changing its 
shape. 

Soon this ameboid body grows in size and begins to develop 
within itself reddish-brown pigment granules. (See Plate XIII. Figs. 
5, 6 and 7). These pigment granules are rapidly moving bodies, and, 
as they are often found in the projections of the parasite, it may look, 
until this fact is corrected by fine focusing, as if several parasites 
were in one corpuscle. As the pigment masses increase, the cor- 
puscle which contains the parasite becomes more and more pale, 
and at the same time swells up or expands, and the ameboid move- 
ments of the parasite grow less and less, while the pigment tends to 
arrange itself toward the periphery. (See Plate XIII, Figs. 7 and 8. 
Finally, only a shell of corpuscle is left (see Plate XIII, Fig. 9), the 
pigment after collecting in the centre becomes motionless, and then 
the parasite undergoes segmentation, there finally developing 10 to 20 
segments, arranged about the central clump of pigment like a rosette. 
Each segment has a spot looking like a nucleus, and soon the spore- 
like bodies so formed break out of their host and attack new and 
previously healthy blood cells. Sometimes the parasite becomes go 
large that it entirely destroys the corpuscle and floats free in the 
blood, in which case the pigment granules quiet down and the mass 
becomes misshapen and apparently dead, breaking up into smaller 
masses, and giving rise to several small bodies, which, however, 
soon seem to lose life (see Plate XIII, Fig. 21), or it becomes filled 
with vacuoles (see Plate XIII, Figs. 23 and 24), or, finally, in drawn 
blood there springs from these extracellular bodies flagella or waving 
arms, extending from the margin of the parasite. (See Plate XIII, 
Fig. 33.) These flagella now and again break off and keep waving 
through the blood, looking like spirilla. The entire process just 
described consumes about forty-eight hours, and it is of interest to 

i The chief American investigators into the life-history of the malarial parasites have been 
Osier, Councilman, Craig, and Thayer and Hewetson, from whose exhaustive and able mono- 
graph of "The Malarial Fevers of Baltimore" much of the information in the text of this book 
is derived. 

2 No 1 is a normal red corpuscle. Plates XIII and XIV are taken from Thayer and Hewet- 
son's monograph. 



398 THE BLOOD 

note that the acme of paroxysm or the disease occurs with the 
segmentation of the full-grown parasite, so that the presence of seg- 
menting bodies indicates the near approach of an attack. If, on 
the other hand, there be a double tertian infection — that is, an 
attack daily — or a quotidian form, there are two sets of parasites, 
which reach their period of segmentation on alternate days, and 
so a daily attack is caused. In such blood during a paroxysm will 
be found two sets of parasites: one set segmenting or causing the 
paroxysm, and the other set half developed, which will produce the 
attack of the morrow. 

The Quartan Parasite, or the one causing an attack every third 
day, in its earlier stages of development looks very much like that 
of the tertian form, for it occurs as a small hyaline ameboid body 
filling a fraction of the corpuscle. It soon, however, develops the 
following differences: First, it possesses a sharper outline; second, 
it is more refractive; third, the ameboid movements are slower 
(Plate XIII, Fig. 26) ; fourth, the pigment granules are coarser and 
darker (Plate XIII, Fig. 27), and, more important still, they lie very 
quietly around the edge of the parasite; fifth, the corpuscle acting 
as host does not increase in size, and finally disappear, as it does 
when affected by the tertian type, but grows smaller and darker, more ■ 
refractive and metallic looking. (See Plate XIII, Figs. 28 to 34.) 
Reaching its complete development in about sixty-four to seventy- 
two hours, it appears as a small round body, taking up nearly all 
the space in the corpuscle in which it lives, or it appears free in the 
blood serum. (See Plate XIII, Fig. 35.) As the time for the paroxysm 
approaches, the pigment granules which have been scattered begin 
to collect at the centre (Plate XIII, Figs. 36 to 39) in a stellate form, 
and the protoplasm of the mass then divides by segmentation into 
from six to twelve small pear-like bodies, each of which has a re- 
fractive centre. These bodies become more and more separated 
from one another, and simultaneously we find new corpuscles in- 
fected by the original small round bodies which we first saw. 

Sometimes these parasites expand and become very transparent, 
their pigment granules become very active, but finally become 
quiet, and the body of the parasite grows more and more indistinct. 
They become dead parasites. (See Plate XIII, Fig. 40.) 

Again, the parasites may undergo a breaking up into smaller 
bodies, which are badly formed and indistinct; a degenerative form 
may also appear, and vacuoles may develop. (See Plate XIII, Fig. 
42.) Finally, flagella may develop, as in the tertian organism (Plate 
XIII, Fig. 41), but they differ from the tertian form in being smaller 
and their granules coarser. 

The Estivo-autumnal Parasite. — In the third form of infection 
(estivo-autumnal fever) we find at first the small hyaline bodies, 






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PARASITES OF THE BLOOD 



399 



hut they have a ringed appearance, and arc sometimes very small. 
(Sec Plate XIV, Figs. 3 to6.) Suddenly this body becomes larger and 
the ring is lost, the edge becoming wavy, and ameboid movements 
occur, the pseudopodia often joining to form a true ring. Pigment 
granules finally develop after a variable length of time, but they are 
few, rarely more than two in a parasite, are near the edge Plate 
XIV, Figs. 7 to 12), and quite still. The corpuscles are not decolor- 
ized, hut often are shrivelled and very brassy looking. 

The peripheral circulation during the paroxysm of estivo-autum- 
nal fever contains very few, if any, parasites, hut blood drawn 
from the spleen may show intracorpuscular parasites, with blocks 
of pigment and some free parasites. As segmentation goes on the 
parasite may look like the tertian form, hut it is far smaller. 
Plate XIV, Figs. 21 to 28.) After this parasite has been present for 
some days we find in the blood larger parasites, of an egg-shape or 
crescent-shape, the remains of the blood cell looking like a "small 
quarter of an apple glued to the side of the crescent," with central 
clumps of pigment granules. It is these bodies which are character- 
istic of estivo-autumnal fever. (See Plate XIV. Fig. 29. Vacuoliza- 
tion and flagellation may develop in this form as in others, and the 
use of quinine in the first week may prevent the development of the 
crescents. 

The following table separates each of these malarial forms from 
the others: 



Tertian Parasite. 

Develops in 48 hours. 
Pale and indistinct. 



Actively ameboid. 

Pigment fine. 

Pigment active in movement. 
Pigment light. 

Corpuscle becomes colorless 
and swollen. 

Full size of the corpuscle. 

Degenerative forms twice as 

large as corpuscle. 
Segments 16 to 20. 



Irregular segments often. 



('uiirtnii l'oiiisitt . 



viumnaJ. 



Develops in 72 hours. 

Sharply outlined and refrac- 
tive. 

Slightly ameboid and later Actively ameboid, 
motionless. 

Pigmenl coarse. 

Pigment slow in movement. 
Pigment dark. 

Corpuscle becomes brassy 
looking and shrunken. 



Develops in 24 t<» 18 bours. 
Baa a winged appearance. 



at grannies are very lew. 

Pigment granules quite still. 



Smaller than the corpuscle. 

Degenerative forms very much 

smaller than in tertian. 
Segments 6 to 12. 



Beautiful rosettes. 



Corpuscle i* shrivelled and 
very brassy, but not decolor- 
ized. 

Very much smaller than a cor- 
puscle. 



The process of segmentation 
goes on in the internal or- 
gans, so segmenting form is 
not found in the peripheral 
blood. 

Forms crescents. 



Craig has directed special attention to a latent human cycle of 
the malarial parasite, the chief feature of which is intracorpuscular 
conjugation. Two of the merozoites or segments of the parasite 
enter a red cell, and, uniting, produce a resting stage resistant to 



400 THE BLOOD 

quinine and other injurious agents. In this stage it remains latent 
until favorable circumstances arise when the parasite segments and 
thus causes a recurrence of the disease. Craig regards this con- 
jugation as the chief cause of the maintenance of malarial infection. 

There is a great difference in the ease with which the various forms 
of the malarial parasite are found in the blood in the peripheral 
circulation. In infection with the tertian parasite, during the later 
stages of development the organism is much more frequently found 
in the blood of the spleen than in the peripheral circulation. In 
cases of quartan infection, the parasites appear in the peripheral 
blood as well as in the spleen, and in the internal organs in all stages 
of development; while in the estivo-autumnal form of the disease, 
only the young forms appear in the peripheral circulation, and when 
the parasites are arranged in groups no organisms may be found in 
the peripheral circulation during the paroxysm. This may also hold 
true in regard to the quartan and tertian parasites, and the entire 
cycle of development may take place in the internal organs, so that 
examination of the peripheral blood may reveal very little. In 
other words, while the discovery of the parasite in a suspected case 
confirms the diagnosis, the absence of the parasite does not abso- 
lutely negative the opinion that it is the cause of the malady. Of 
course, a very considerable number of slides should be carefully 
examined before it is stated that malarial parasites cannot be found. 
Given a case in which a considerable number of parasites are found 
in the peripheral circulation, we have a right to infer that the infec- 
tion is severe. But this does not necessarily follow. 

It has already been stated that the paroxysm of the malarial dis- 
ease takes place at the time when the parasite is breaking up into 
segments. In other words, the attacks occur whenever the cycle of 
growth of a set of parasites is completed, which in tertian fever is 
every forty-eight hours and in quartan fever every seventy-two 
hours. If there be two sets of parasites in the blood, however, of 
the tertian type, the attacks may be daily, or quotidian, since each 
set matures on alternate days. This is often called double tertian. 
The tertian is the most common form of the disease in the United 
States. If there be a double quartan infection, the attacks come on 
two successive days, then a day of intermission ensues. If three sets 
of parasites of this type are present, the attacks may be daily for 
three days — triple quartan infection. (See chapter on Fever.) 

The parasite of estivo-autumnal fever is often very irregular in its 
development, and is often the cause of the irregular malarial fever 
seen in the fall of the year. It yields less readily to quinine than 
the others, and is the usual cause of the pernicious types of the 
disease. 

From what has been said it can readily be seen that the best time to 



PARASITES OF THE BLOOD 401 

examine the Mood for the parasite is a short time before the paroxysm 

is expected, as then the fully developed forms, easily recognized 
even by the novice, are present. Occasionally during or after the 
paroxysm is the better time. In some of the chronic or irregular 
infections, repeated examinations of the peripheral blood fail to 
reveal parasites which may be detected in blood obtained by splenic 
puncture. 

Malarial infection differs from most infections, the symptoms of 
which resemble it, in that there is no increase in the leukocytes, 
whereas in sepsis a great increase is usually present. In fact, then- 
is often a distinct decrease in the number of leukocytes with a relative 
increase of the large mononuclears. This gives us an important 
aid in differential diagnosis. (See chapter on Fever.) When the 
malarial organisms cannot be found the presence of leukocytes 
bearing pigment granules may indicate the breaking down of the 
red cells by the parasite, and so point to the probable presence of 
malaria. 

Changes in the red cells and hemoglobin may be pronounced. 
In severe acute malarial infection, the red cells may within three or 
four weeks fall to 1 ,000,000 or less, the hemoglobin usually to a greater 
degree. In some cases the extensive hemolysis is evidenced by pro- 
nounced hemoglobinuria. In chronic cases anemia is often profound. 

Staining the Parasites. — In examining the blood for the estivo- 
antnmnal parasite, it will often be found that the best results arc 
obtained if the blood is stained. For while, as a rule, the examina- 
tion of a fresh specimen, prepared in the manner already described, 
is the best method of examining the blood for the malarial parasite. 
it is a fact that it is difficult to discover the small hyaline forms in 
a fresh specimen. Under these circumstances Thayer recommends 
Nocht's modification of Romanowsky's stain. This method is as 
follows : 

Polychrome methylene blue is carefully neutralized. This is 
done by first adding dilute acetic acid until the solution is acid. 
When litmus paper is dipped into the solution, it is colored by the 
methylene blue, but on the margin of the moist portion the acidity 
causes a red line to appear. The solution is now brought back to 
the neutral point by the addition of more polychrome methylene 
blue until the red line fails to appear on the blue litmus paper. The 
polychrome methylene blue may be obtained already prepared 
It can, however, be readily made by heating for several hours, on a 
water-bath, a solution consisting of: 

Methylene blue 1 part. 

Caustic soda 1 part. 

Water (distilled) 100 parts. 

After cooling, the solution is to be filtered. 
26 



4()2 THE BLOOD 

To this polychrome methylene blue an equal quantity of distilled 
water is added, and then a saturated solution of ordinary methylene 
blue until the red color is completely lost, the solution appearing 
simply blue. For this purpose, about 1 part of the saturated aqueous 
solution to 10 parts of the diluted polychrome solution will be used. 

A solution of eosin is now prepared, according to Nocht, by 
adding 3 or 4 drops of a 1 per cent, aqueous solution of eosin to 1 or 
2 c.c. of water. This is practically a 0.2 per cent, solution; it can be 
made up in quantity. To 3 or 4 c.c. of the eosin solution, Nocht 
adds the methylene-blue solution until the red color disappears. At 
this point a fine precipitate is thrown down, and a scum begins to 
form on the surface. 

Thayer also advises that the eosin and methylene blue be mixed 
immediately before being used, and the mixture used only once, since 
when it is kept a day or two, though it gives the chromatin stain, it 
is but feebly. The best method of fixing the blood smears for this 
stain is to treat them with 0.25 per cent, solution of formalin in 95 
per cent, alcohol for one or two minutes. When this stain is used, 
the hyaline forms of the parasites appear as delicate blue rings, the 
central part being occupied by a large colorless nucleus, at one side 
of which is a small spot of chromatin substance, which stains a 
deep carmine violet. 

Any of the polychrome methylene blue-eosin combinations men- 
tioned for general blood work answers well as a routine stain for the 
malarial parasite, though by some of them the chromatin is not 
sharply differentiated. For this the method of Giemsa is probably 
the best. Whatever method be employed, the stain is applied to 
thin films of blood prepared as described for the study of the cor- 
puscles of the blood. 

The Development in the Mosquito . — The bodies which are cres- 
centic and those which are ovoid are not capable of sporulation, 
and are called gametocytes. While they are incapable of develop- 
ment in the human being, in the definitive host, the mosquito, or 
even on the slide of the microscope, the microgametocytes or male 
elements give off a number of long motile flagella (microgametes), 
which, breaking loose, penetrate and fecundate the female forms, 
or the macrogametes. This fecundated female form now enters 
the wall of the stomach of the mosquito, where it begins devel- 
opment within forty-eight hours; there then develops in the 
stomach wall of the mosquito small, round, refractive bodies of 
granular appearance, and which contain pigment granules. Five 
days later these bodies develop stride, due to the development of 
sporoblasts, and finally the original organism or mother oocyst 
bursts, and sets free a multitude of small sporoblasts, which find their 
way into the venenosalivary glands of the mosquito, and from there 
pass into the body of the bitten patient, where they enter red cells a;3 



P Ale A SITES OF THE I; LOO I) 



403 



young parasites. The shapes other than those which arc crescentic 
or ovoid have an asexual development and infect new blood cells 
without having to pass into the body of the mosquito. The Ano- 
pheles is the only mosquito which is known to act as a host in the 
way described. It occurs in several forms in the United State-. 
the most common being the Anopheles auadrimaeulatus, which is 
identical with the Anopheles claviger or macidipennis of Europe. 

This mosquito is to be separated from the other mosquitoes by the 
following points: The wings are mottled, the posterior pair of legs 
is nearly parallel to the wall on which the insect rests, although they 
may be lifted over the back, in the same manner as does the Culex. 
The body, instead of being parallel with the resting surface, is at an 
angle of 45 degrees, whereas, the body of the non-malarial mosquito 
rests parallel with this surface (Fig. 1(33). 




Fig. 163. — The picture to the left represents the Culex or non-malaria-bearing mosquito at 
rest. The figure to the right shows the resting attitude of the Anopheles quadrimaculatus. 
(Modified from drawing in the British Medical Journal.) 



Filaria. — The Filaria sanguinis hotninis appears in the blood 
in its embryonal form, and is found fully developed only in the lym- 
phatics. It occurs in three forms. These forms are: (1) Filaria 
diurna; {2) Filaria noetuma; (3) Filaria per starts. These names 
are indicative of the habits of the animal, the filaria diurna being 
found in the superficial vessels solely or chiefly during the day; the 
Filaria noetuma solely or chiefly during the night; while the Filaria 
perstans is constantly present in the capillaries of the integument. 
The Filaria diurna and Filaria perstans are confined, thus far, to the 
west coast of Africa and adjoining districts, while the Filaria noetuma 



404 



THE BLOOD 



is pandemic in the tropics and endemic in certain sections of the 
United States. The adults of Filaria nocturna have been frequently 
found ; that of Filaria perstans never, so far as Henry has been able to 
ascertain. Manson has also described another parasite, the Filaria 
demarquai, which is less than half the size of the Filaria nocturna, 
and another form which he calls the Filaria ozzardi. In the opinion 



w* 




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Fig. 164. — Filaria alive in the blood. Instantaneous photomicrograph. Four hundred 
diameters' magnification. Four millimeters Zeiss apochromatic. (Henry's case.) 



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Fig. 165.— Filaria in the blood. Eight hundred diameters. (Henry's case.) 

of Manson, the Filaria loa, found chiefly in the eye of the negro of 
Old Calabar, is probably the adult form of the Filaria diurna. If 
it is not, he argues, then there must be another blood worm yet to 
be discovered, for the embryos of the loa must escape from the body 
of their host through the medium of the circulation. 

The second variety, or nocturna, is the one ordinarily seen in blood 



PARASITES OF THE BLOOD 405 

obtained from the peripheral circulation during sleep or at night 
(Figs. L64 and 165). The adult male filaria measures 83 millimeters 
long by 0.407 millimeter broad, and the tail is twisted into a spiral 
form. The female measures 155 millimeters long by 0.715 milli- 
meter wide, and the vulva is 2.56 micromillimeters from the anterior 
extremity. The adult parasite is found only in the lymph vessels. 
The embryo, which is found in the circulating blood, measures 270 
to 1)40 micromillimeters long by 7 to 11 mieromillimeters wideband 
has a pointed tail. This embryo is in an almost imperceptible shell, 
which does not impede its movements, and as it is about the diameter 
of a red blood corpuscle it passes through the capillaries in extra- 
ordinary numbers. Its active movements and typical appearance 
render it readily seen in the blood. The discovery of this parasite 
in the blood renders a diagnosis certain, and it should always be 
sought for if chyluria or elephantiasis is present. If the patient 
remains awake at night and sleeps during the daytime the organism 
will be found in the blood during the sleeping period. 

The Filaria diurna is found in the blood during waking hours. 
The embryos of the Filaria perstans are the only form of this parasite 
known. 

Trypanosoma. — This parasite, like the filaria, does not enter the 
blood corpuscles. It is a flagellate, in length two or three times, in 
width one-third, the diameter of a red blood cell. It possesses an 
active, screw-like motion imparted by an undulating membrane 
continuous with one border of the parasite and a single flagellum 
projecting anteriorly. It can be readily recognized in fresh blood 
by the aid of low powers of the microscope and in films is well shown 
by polychrome methylene blue-eosin stains. Various species of this 
parasite are found in the blood of many small animals and also in 
horses and cattle. The Trypanosoma garribiense is pathogenic for 
man and infests great numbers of the natives in some of the West 
African States. A number of Europeans have also contracted 
the disease. The parasite is transmitted by a fly, the Glossina 
palpalis. 

Clinically, the infection is chronic in type, first characterized by 
circulatory and respiratory disturbances, irregular fever, multiple 
areas of edema and erythema, enlargement of the spleen and lymph 
glands, emaciation, and progressive loss of strength. During this 
period the parasite is found in the blood, usually in small numbers, 
and in the fluid from the affected lymph glands. Later, the parasite 
enters the cerebrospinal fluid, giving rise to the well-known "sleeping 
sickness," which is uniformly fatal. The trypanosoma may be 
demonstrated in the sediment obtained by centrifugalizing spinal 
fluid obtained by lumbar puncture. The blood picture in this 
infection is that of a moderate anemia with normal or reduced 



40G THE BLOOD 

number of leukocytes, showing a relative increase of the large 
mononuclear forms. 

Widal's Test for Typhoid or Enteric Fever depends upon 
the fact that the blood serum of a patient suffering from typhoid 
fever exercises an agglutinative effect upon the typhoid bacillus. The 
microscopic method is as follows: The lobe of the patient's ear 
having been pricked, the drop of blood is placed on a clean glass slide 
and allowed to dry. A loop of twenty-four-hour bouillon culture 
inoculated from a twenty-day agar growth of the typhoid bacillus is 
now placed on an absolutely clean cover-glass, and to this is added 
a large loopful of a watery solution of the dried blood. From the 
mixture of blood and typhoid bouillon a " hanging-drop" preparation 
is made, and examined with \ or J dry objective, when it will be 
noticed, if the patient is suffering from typhoid fever, that the typhoid 
bacilli rapidly form clumps and become non-motile. If the patient 
has not typhoid fever, this clumping and entanglement of the bacilli 
with arrest of their movements does not take place, unless he has 
had the disease within several months, when the reaction may occur 
without signifying the onset of a new attack. Partial clumping is 
not to be considered indicative of a positive test. By this method 
accurate dilution cannot be made, hence if uniformity is to be secured 
the fresh blood should be at once diluted with distilled water, best 
in a hematocytometer pipette, 1 to 20, as a dilution of 1 to 40 with 
the bouillon culture is commonly employed. With this dilution, 
if the reaction be not completed or well advanced in thirty minutes, 
the test should be considered negative. Fairly satisfactory macro- 
scopic methods for performing this test have also been devised. 

This test has now been placed within the reach of practitioners 
who have not laboratory facilities by an apparatus marketed byParke, 
Davis & Co. By its use the necessity of the microscope and the 
fresh live culture of typhoid bacilli are obviated. A bottle of sterile 
permanent suspension of typhoid bacilli is provided together with 
four test tubes, a lancet and a tube for collecting blood. With this 
is one vial for diluting the blood serum, one small pipette for dis- 
tributing the diluted serum, and one large pipette with two gradua- 
tions (each corresponding to 10 drops of the size delivered by the 
small pipette) for filling the tubes with suspension. The three tubes 
labelled 50, 100, and 200 are to be used for the test. The fourth 
tube is employed as a control tube and no serum is added to it. 

The blood is allowed to flow into the blood tube until the bottom 
is covered with a layer one-eighth to one-quarter inches thick. The 
blood will flow much more rapidly if the lobe of the ear is squeezed 
intermittently between the thumb and index finger. 



PARASITES OF THE BLOOD 



40; 



Cork the tube and replace in an upright position. 

In a short time (an hour) the serum will have separated, or may 
be readily made to do so by carefully loosening the edges of the clot 
with the lancet. 

After the serum has separated, insert the pipette into the blood 
tube, the point resting in the lateral depression, and incline both 
slightly, when the serum will readily enter the pipette. 

Add 1 drop of serum to 10 drops of clear water in the diluting 
tube, and shake well. If the diluted serum is cloudy, let it 
clear by standing a few minutes before distributing to the tubes 
of suspension. 

By means of the large pipette put 20 drops (two graduations) of 
the suspension of typhoid bacilli in each of the four test tubes. 




Fig. 166 



8| Add the serum dilution to the typhoid suspension in the following 
amounts: Four drops added to the tube marked 50 give a dilution 
of 1 to 50; 2 drops added to the tube marked 100 give a dilution of 
1 to 100; 1 drop added to the tube marked 200 gives a dilution of 
1 to 200. 

No serum should be added to the control tube. 

After adding the serum dilution, cork the tubes and shake well. 
Put away in a warm place. 

Examine the tubes at the end of one and four hours, and again on 
the following day. The rapidity of the reaction depends both upon 
the agglutinating pow T er of the blood serum and the temperature at 



408 THE BLOOD 

which the tubes are kept. The reaction may be seen with the great- 
est distinctness when one stands near the middle of the room facing 
a window. The tubes should be held on a level with the eye and 
inclined slightly away from the observer. 

When the reaction is positive, floccules appear in one or more of 
the tubes, depending upon the agglutinating power of the serum 
tested. These flakes are small at first and disseminated through 
the fluid. They gradually increase in size and settle to the bottom 
of the tube. 

In a complete reaction the supernatant fluid is perfectly clear. 

In the positive but incomplete reaction, floccules are seen in the 
still cloudy fluid. 

In a negative reaction, the fluid in the tubes remains uniformly 
clouded, as in the control. 

All apparatus and corks should be thoroughly washed before 
using a second time. 

The Widal test varies in the constancy of its development with 
the stage of the disease, being most marked in the third and fourth 
weeks. In a large series of cases Park found it present in 20 per 
cent, of cases in the first week, 60 per cent, in the second week, 80 
per cent, in the third week, 90 per cent, in the fourth week, and in 
75 per cent, at the end of two months. The chief difficulty with this 
test, therefore, is that it fails to appear at a time when the diagnosis 
is often most difficult, namely, in the first few days of the illness. 

Sugar in the Blood. — The blood in persons suffering from 
diabetes contains sugar in excess, and R. T. Williamson has sug- 
gested its discovery by the following process. The normal blood 
will not give this reaction. A small, narrow test-tube is well cleaned, 
and at the bottom of the tube are placed 40 c.mm. of water. To 
measure this the capillary tube of a Gowers hemoglobinometer is 
used, which is graduated for 20 c.mm. The tip of one of the patient's 
fingers is cleaned and dried, then pricked, and when a large drop of 
blood has escaped it is sucked up into the small capillary hemo- 
globinometer tube. 21 c.mm. of blood are taken up from the finger. 
The blood is then blown gently into the water at the bottom of the 
small test tube. If it should adhere to the side of the tube, it 
must be carefully shaken to the bottom. Then 1 c.c. of a 1 in 6000 
watery solution of methylene blue is added. Finally, there is added 
to the mixture 40 c.mm. of liquor potassa. The contents of the tube 
are then well mixed by shaking. As a control experiment a second 
test tube of similar size is taken, and into this is placed the same 
quantity of non-diabetic blood, with the same proportion of water, 
methylene blue, and liquor potassa. 



PARASITES OF THE BLOOD 409 

The fluid in each tube has a fairly deep-blue color. Both tubes 
are then placed in a beaker or capsule containing water. This is 
heated over a spirit lamp until the water boils; it is allowed to con- 
tinue boiling for about four minutes. By the end of this time the 
fluid in the tube containing the diabetic blood lias changed its color 
from fairly deep blue to a dirty pale yellow (almost the color of nor- 
mal urine), while the fluid in the tube containing the non-diabetic 
blood remains blue, or occasionally becomes bluish green, sometimes 
pale violet, but is never decolorized — that is, it never entirely loses 
its blue color. The tubes should be kept quite still while in the 
water-bath, as by shaking the decolorized methylene blue is oxidized 
by the oxygen of the atmosphere, and a blue tint may then return to 
the fluid. This is the reason why it is necessary to use a water-bath, 
since if the test tubes be heated directly over the spirit lamp it is 
difficult to avoid shaking the fluid. 

Opsonic Index. — A method of testing the blood for the purpose 
of determining its ability to aid the body in combating infection has 
been devised by Wright, and depends upon the presence of something 
in the blood serum which so influences invading organisms that the 
leukocytes can destroy them by phagocytosis. This something, 
which has not yet been isolated, is given the name of "opsonin;" the 
word "opsonin" being derived from the Greek, meaning "To cater 
for," or "to prepare food." In other words, an opsonin affects the 
microorganism in such a way that the leukocytes can devour them. 
In those individuals who are susceptible to infection, a condition has 
arisen which has impaired or destroyed the opsonic activity of the 
serum. The test to determine the resistance of an individual to 
bacterial invasion consists in comparing the activity of the leukocytes 
of the patient in devouring the bacteria, when these bacteria are 
exposed to his own serum, with the activity of the leukocytes when the 
microorganism is exposed to the influence of the serum of a normal 
individual. If each polymorphonuclear leukocyte exposed to the 
normal serum contains on the average 2 bacteria, the phagocytic 
index is said to be 2. If each leukocyte of the patient contains 1 
bacterium, his phagocytic index is said to be 1. The phagocytic 
index of the blood to be tested divided by the phagocytic index of 
the normal serum is called the "opsonic index." This test has not 
been studied long enough to determine its value, but promises much 
both for diagnosis and therapeutics for two reasons. It is, however, 
valueless except in the hands of the most expert, and even then may 
give variable results. In diagnosis it aids us in determining not only 
the vital resistance of a patient, but, in addition, the exact nature of 
his infection, because if he has any vital resistance, in the course of 
time the opsonic index in his serum for a particular infecting germ 



410 THE BLOOD 

rises to meet the needs of the individual in resisting the invading 
microorganisms. So, too, it is possible by the introduction into 
the body of a carefully prepared product, or vaccine, of a definite 
microorganism to so stimulate the development of the opsonin as to 
enable him to still better combat infection. 

In resorting to opsonic therapy it is important that the germ 
causing the particular condition to be treated be isolated and that 
the vaccines be prepared from cultures so obtained. 



CHAPTER XIII. 

THE EYE. 

The general diagnostic indications afforded by the eye -Diplopia and disorder 
of the external ocular muscles Strabismus and squint — Disorder of the 
internal ocular muscles The pupil Hemianopsia -The visual fields 
Color vision — The optic nerve and it- Lesions— Retinitis -Amblyopia and 

blindness. 

The eye affords more information for diagnostic purposes con- 
cerning the condition of other organs of the body than any single 
pari which can be examined. We gather from it not only a clear 

idea as to its own state, and the state of the nervous centres more 
or less intimately connected with the government of its movements 
and its special functions, hut in addition we often gain positive 
information as to the condition of organs more remotely situated, 
as, for example, the kidneys. The very fact that so many different 
tissues are found in this organ renders it susceptible to the many 
diseases affecting similar tissues elsewhere in the body. The parts 
of the eye which give us the greatest amount of knowledge about 
changes in other tissues are the optic nerve and retina and its vessels 
and the ocular muscles. The crystalline lens, the conjunctiva, and 
the cornea often give additional evidence indicating the general 
systemic condition. Cataract should make the physician suspect 
diabetes, even if it appear in persons advanced in years. The eyelids, 
if puffy in appearance, may indicate renal disease, cardiac lesions, 
or the overuse of arsenic. (See chapter on the Face.) An exami- 
nation of the inner side of the lids may reveal a pallor due to anemia. 
Slight conjunctival hemorrhage may result from violent coughing. 
and when it is recurrent it should arouse the suspicion of renal 
disease with secondary vascular troubles. In old persons such a 
hemorrhage, if not due to injury, may indicate degenerative vascular 
changes. 

Prominence of the eyeball, or exophthalmos, is seen as an almost 
constant symptom of true goitre, which for this reason is called 
cxoplitlialmic goitre. (See Fig. 8.) Associated with the bulging 
eveball we find more or less enlargement of the thyroid gland, an 
irritable heart, and a very rapid pulse, throbbing carotid arteries, 
marked general nervousness, often mental depression, and insomnia. 
In well-marked or advanced cases of exophthalmic goitre we often 



412 THE EYE 

have a condition in which the upper eyelid does not follow the eyeball 
in its downward movement. This is sometimes called "Graefe's 
symptom." Again, the lids may so imperfectly cover the eye that the 
sclera can be seen above and below the cornea, "Stellwag's symp- 
tom." Or, again, there is insufficiency of convergence, so that a 
near point cannot be seen with both eyes at once (Moebius' sign). 

On examining the exterior of the eyeball we often notice a grayish 
ring along the junction of the cornea and sclera. It possesses, when 
a complete ring, but little significance, except age; but if it is the 
segment of a ring or in two segments, at the upper and lower margins 
of the cornea, it is a true arcus senilis, and is said to indicate in some 
cases fatty degeneration of the tissues of the body. The one is an 
annulus senilis, the other an arcus senilis, and the arcus is the change 
worthy of note, although many clinicians, including the author, deny 
that either has much significance. 

An examination of the pupil may reveal that it is immobile from 
an old plastic iritis, due to syphilis or rheumatism, but it is not to 
be forgotten that this condition may arise from iritis due to purely 
local causes. A widely dilated pupil may indicate the use of some 
mydriatic or the ingestion of atropine. Such a pupil is also seen in 
fright, in some hysterical seizures, and in glaucoma and whenever 
the vision is lost, unless the pupil be contracted by disease of the iris. 
A contracted pupil indicates the use of a myotic or the existence of 
central nervous disease, such as ataxia, which causes the Argyll- 
Robertson pupil as well. Sometimes corneal inflammation by causing 
photophobia may cause excessive myosis. Pin-point pupils may 
also result from the use of opium or its alkaloids, and serve to differ- 
entiate the condition from true coma, in which the pupils are usually 
dilated. If, however, the coma be due to cerebral inflammation or 
meningitis, the pupils may be contracted; or if it be due to intra- 
cranial pressure, they are usually dilated. (See Paralysis of the 
Intraocular Muscles.) 

In addition to these objective symptoms we have also a very impor- 
tant set of signs connected with the ocular muscles, external and 
internal, as manifested by the various forms of strabismus or changes 
in the pupil and in the accommodation of the eye, by the ptosis 
already discussed in the chapter on the Face, and in nystagmus and 
ocular spasm. (See later pages.) Beyond this, too, we have two 
other ocular symptoms subjective in nature, namely, diplopia, or 
double vision, and partial or complete blindness. 

Diplopia depends upon the fact that in an eye in which the muscles 
are abnormal in their function the image which falls upon the fovea, 
or visual acuity spot of the retina, in the well eye fails to fall upon 
the same spot in the weak eye. To the well eye the object appears 
to be in the direction in which the eye is turned, whereas to the weak 



PARALYSIS OF EXTRA OCULAR MUSCLES 413 

eye if appears to be in another direction. As a result, the mind gets 
the impression of two objects instead of one. The impression made 
on the well side is the "true image," as it is called, and that in the 
diseased eye is called the " false image." Any cause which interferes 
with the fixation of* each eye on the same poinl produces diplopia, 
and, as the eyes are normally directed to the object fixed by the 
ocular muscles, paralysis of any one of these muscles produces 
diplopia when the axis of one eye is deviated from the point of fixa- 
tion, because the eye on one side is not properly moved by reason of 
the fact that one muscle has failed. Diplopia is ordinarily a constant 
sign of ocular muscular paralysis; l>nt if only weakness or insuffici- 
ency of a muscle is present, diplopia may never he a symptom recog- 
nized by the patient. The forms of diplopia that is, the position of 
the false images in respect to the true images— vary with the muscles 
affected, and will he studied (see below) when paralysis of the 
muscles is tested for and their diagnosis discussed. It only remains 
at this place, therefore, to point out the probable significance if a 
patient with diplopia presents himself to a physician. 

Thus, a patient with diplopia may he suffering from a lesion in 
the cerebral cortex, such as hemorrhage, sclerosis, or softening; or 
from a lesion in the cranial nerve nuclei, in the pons or corpora quad- 
rigemina, or in the fascicular fibers. Again, diplopia may arise from 
lesions at the base of the brain, as meningitis, tuberculous or syphilitic, 
or from injury to the nerves in the orbit or in their peripheral ending. 
As a result, we find diplopia as a symptom of any disease which may 
affect these parts, and it is quite a common symptom in locomotor 
ataxia, in Friedreich's ataxia, and in paretic dementia. Probably 
it is seen most commonly in ataxia, and with it, as the oculomotor 
nerve in its branch supplying the levator palpebral is particularly 
apt to be paralyzed in this disease, we may find ptosis. 

Diplopia is also found in cases of ptomai'n poisoning, and in 
poisoning by belladonna, spigelia, conhun, and gelscinium, owing 
to their effects on .the ocular nerves. 

The differential diagnosis between the various lesions producing 
diplopia is to be made by the other symptoms and the history of 
the case. 

Paralysis of Extra-ocular Muscles. — As something has already 
been said in the chapter on the Face and Head of the diagnostic 
import of paralysis of the ocular muscles in connection with the 
subject of ptosis, a further consideration of the abnormal changes in 
their functions will be discussed first in the present chapter. 1 Before 
doing so, however, it is necessary to describe the methods resorted 
to for the purpose of demonstrating or determining departures from 

iln the preparation of this chapter tree use has been made of the article of my friend, 
Dr. de Schweinitz, on " Diseases of the Cranial Nerves, in Dercum's "Nervous Diseases." 



414 THE EYE 

the normal in these muscles. In the first place, it must be clearly 
understood that the function of the extrinsic muscles of the eyeball 
is to direct the ball toward the object at which the patient desires to 
look, and also evenly balance one another to keep the eye steady 
in its axis. Thus, the external and internal rectus muscles maintain 
the horizontal equilibrium of the eyeball. If the internal rectus is 
completely paralyzed in one eye, we have developed a unilateral 
external squint, the eye looking toward the outer side of the orbit; 
and if the external rectus fails, the eyeball is turned toward the nose. 
If these muscles are affected in both eyes, we have a divergent squint 
in the first case and a convergent squint in the second. Not only 
do the muscles of each eyeball govern the eye movements of that 
side, but by the nervous centres governing the eye muscles the two 
sets of eye muscles are coordinated, so that they move as one organ 
in health. 

Just here it is well for the reader to make a clear distinction 
between concomitant and paralytic squint, for they are two very 
different things in origin, symptoms, course, and prognosis. A con- 
comitant squint is a wrong relation in the visual axes, so that they 
do not intersect in the point looked at; but there is no marked limita- 
tion of the movements of either eye in any direction. Be the direction 
of the eyes what it may, the squint remains practically unchanged. 
Further, if the fixing eye is covered, the other eye promptly fixes, 
and the covered eye deviates without the patient altering the position 
of the eye. (Jackson.) On the other hand, paralytic squint is the 
deviation which takes place when the attempt is made to turn the 
eyes in certain directions by means of the muscles which are paralyzed 
in whole or in part. When the attempt is made, the eye with the 
sound muscles turns as it should, while the eye with a paralyzed 
muscle hangs back, beginning to deviate as the eyes are turned, so 
that this muscle is required to perform its function, and deviates 
more as greater effort is required. The degree of squint and of sepa- 
ration of the double images it causes varies with the direction in 
which the eyes are turned, there being none at all in certain directions. 

We examine the functional activity of the ocular muscles by the 
following measures: 

The patient is told to look at the tip of a pencil or the tip of the 
finger of the physician, held about three feet from his face. This 
object is then gradually brought nearer and nearer to him, and 
the eyes of the patient necessarily converge more and more as it 
approaches his nose. Normally the eyes will be coordinately con- 
verged when the object is only three and a half inches from them; but 
if any weakness or insufficiency of one internus is present, the eye on 
that side will deviate or fail to converge before this point is reached. 

Again, a fine point like a pin-point is held at about eight or ten 



IW/fALVS/S OF EXTRA OCULAR MUSCLES 



415 



inches from the eyes and below the horizontal, and one eve is covered 
by a card or hand. If the eye which is separated from the object by 
the card deviates inward, it indicates insufficiency of the external 
rectus. If, on the other hand, it deviates outward, it shows insuffi- 
ciency of the internal rectus. On sudden removal of the card the 
eye at once springs back into place for the purpose of fixing upon the 
object, and "in general terms each millimeter of movement deviating 
from the fixation point corresponds to what is called 2° of insuffi- 
ciency, as measured by prisms." (Randall.) If the interims is 
insufficient, and the covered eye moves in to fix in several distinct 
impulses, each impulse should be multiplied into the foregoing result. 
A very useful, and the simplest, apparatus for testing the func- 
tional balance of the ocular muscles is the rod tesl of Maddox. 




Fig. 167. — Maddux's rod test for horizontal deviation. The rod is before the right eye. A. 
The line passes through the flame — orthophoria. B. The line passes to the right of the flame 
— latent convergence, or esophoria. C. The line passes to the left of the flame — latent diver- 
gence, or exophoria. (de Schweinitz.) 

A cell in which is mounted a transparent glass rod is placed in a 
trial frame, which is then placed in front of the eyes. If the hori- 
zontal deviation is to be determined the physician should "seat the 
patient at six meters from a small flame, and place the rod horizon- 
tally before one eve, a colored glass before the other. If the line 
passes (vertically) through the flame there is orthophoria (equipoise), 
as far as the horizontal movements of the eyes are concerned. Should 
the line lie to either side of the flame, as in most people it will, there 
is either latent convergence or latent divergence: the former if the 
line is the same side as the rod (homonymous diplopia), the latter 
if to the other side (crossed diplopia) (Fig. 167). 

When the vertical deviation is to be estimated the rod is placed 



416 



THE EYE 



vertically in the frame. If the patient states that the horizontal line 
of light passes directly through the flame, the vertical balance of the 
eyes is normal; if, on the other hand, the line is above the flame, 
there is a tendency to upward deviation of the naked eye; but if the 
line is below the flame, there is upward deviation of the eye covered 
by the rod test (Fig. 168). Testing of this kind refers to the 
insufficiencies and not to the palsies of the ocular muscles. 

The importance of being able to demonstrate these minor failures 
in the ocular muscles by these means lies in the fact that in this 
manner headaches due to muscle eye-strain may be remedied by 
removing their cause by properly fitted glasses, or by gymnastic 
exercises with prisms, or in some cases by tenotomy. 




Fig. 168. — Maddox's rod test for vertical deviation. The rod is before the right eye. A. The 
line passes through the flame — orthophoria. B The line passes helow the flame. The upper 
image belongs to the left eye — right hyperphoria. C The line passes above the flame. The 
upper image belongs to the right eye — left hyperphoria, (de Schweinitz.) 

Where there are marked palsies of the ocular muscles, there is 
usually some poison exercising its effects upon their nervous centres 
or the nerves themselves, or there is some central nervous lesion 
affecting the centres governing these muscles in the cortex, or there 
is a lesion in the nuclei or fasciculi, or, again, there may be lesions 
in the basal ganglia, or in the course of the fibers of the nerve between 
the nucleus and the eye, or in the orbit or nerve endings. 

The signs of paralysis of the ocular muscles consist in the follow- 
ing symptoms: Diplopia, which is due to the failure of the images 
to fall on the corresponding points in each retina. This diplopia 
becomes more and more marked as the object moves toward the side 
on which the paralyzed muscle lies. Strabismus, which may or may 
not be constant, usually develops when the patient endeavors to 
turn his eyes in the direction of the paralyzed muscle. Vertigo, which 



PARALYSIS OF EXTRA OCULAR Ml SCLES 417 

is due to the diplopia, or, if the well eye is closed, to an erroneous 
localization of the objects in the field of vision. Altered carriage 

of the head, due to the factjthat the patient tries to turn his head in 
the direction in which he is least troubled by double images — that 
is, he obtains the natural fixation point of the weak eye, and then 
adjusts the well eye accordingly. 

If the paralysis of the ocular muscle be complete, the squint and 
the loss of movement of the muscle which is paralyzed will usually 
enable the physician to find out the paralyzed muscle; but if there 
be only a partial paralysis or paresis of an ocular muscle, then squint 
is not necessarily present, and the diagnosis of the part affected must 
be made by a study of the double images. This is made by placing 
before the patient, at a distance of from three to live yards, a candle 
on the same level as his eyes. One eye is covered by a piece of red 
glass, so that the patient can readily distinguish between the images. 
The lighted candle is then moved from the middle of the patient to 
the right and left, and the relative positions of the red and white 
images are noted. Then the candle is moved up and down, and the 
results recorded. These operations having been recorded, it is to 
be remembered that diplopia is most marked and sometimes only 
appears when the patient turns his eyes in that direction which calls 
into play the affected muscles, no diplopia being present if other 
muscles are used. Again, the image which belongs to the affected 
eye is projected in the direction toward which the paralyzed muscle 
normally turns the eye, and, finally, the distance of the double image 
increases when the eyes are turned in the direction of the action of 
the paralyzed muscle, or, in other words, that image is false and 
belongs to the affected eye which in the region of diplopia moves 
faster than the moving test object — that is, the candle flame. 

If there is divergent squint with failure of movement in all 
directions, except outward and slightly downward, and there are 
ptosis, moderate mydriasis, and paralysis of accommodation, there 
are oculomotor paralysis and crossed diplopia. 

The following table of Hotz (International Clinics-, vol. hi, fourth 
series) summarizes the facts as to the diagnosis of the conditions 
producing strabismus: 

I. Lateral diplopia indicates paralysis of an internal or external 
rectus. 

1. Homonymous diplopia indicates paralysis of an external 
rectus. 

(a) Images separating to the right indicate paralysis of the 
externus of the right eye. 

(b) Images separating to the left indicate paralysis of the 
externus of the left eye. 

2. Crossed images indicate paralysis of an internus. 
27 



418 THE EYE 

(a) Images separating to the right indicate paralysis of the inter- 
ims of the left eye. 

(6) Images separating to the left indicate paralysis of the inter- 
nus of the right eye. 

II. Vertical diplopia in the upper field indicates paralysis of the 
superior rectus or inferior oblique. 

1. Homonymous images indicate paralysis of the inferior oblique. 
(a) Image of right eye higher means paralysis of the inferior 

oblique of the right eye. 

(6) Image of right eye lower means paralysis of the inferior 
oblique of the left eye. 

2. Crossed images indicate paralysis of the superior rectus. 

(a) Image of right eye higher means paralysis of the superior 
rectus of the right eye. 

(b) Image of right eye lower means paralysis of the superior 
rectus of the left eye. 

III. Vertical diplopia in the lower field indicates paralysis of the 
inferior rectus or superior oblique. 

1 . Homonymous images indicate paralysis of the superior oblique. 
(a) Image of the right eye higher means paralysis of the superior 

oblique of the left eye. 

2. Crossed images indicate paralysis of the inferior rectus. 

(a) Image of the right eye lower means paralysis of the inferior 
rectus of the right eye. 

(b) Image of the right eye higher means paralysis of the inferior 
rectus of the left eye. 

It is exceedingly difficult, however, always to localize exactly the 
affected muscle, a difficulty which is much increased when more 
than one is paretic, the paresis being of different degrees. 

Paralysis of the ocular muscles may be due to a lesion in one of 
several places. Thus it may arise from hemorrhage, sclerosis, and 
softening of the cerebral cortex, in which case the other symptoms 
of lesions in those parts will be present as in apoplexy, disseminated 
sclerosis, or meningeal disease. Or it may depend upon lesions in 
the fasciculi between the cortex and the nuclear origin of the nerves, 
as in the crus. This is rare. Or, again, it may be due to lesions 
in the nuclei. If this be the case, we have developed ophthalmo- 
plegia, 1 or paralysis of all the ocular muscles supplied by the third, 
fourth, and sixth nerves. This nuclear paralysis is divisible into 
two classes, the acute and chronic. Sometimes it is called acute and 
chronic nuclear palsy. The acute form is sudden in its onset, all the 
ocular muscles losing power. With the onset of the attack there may 

1 Ophthalmoplegia is here applied in its strict sense. The word is often used to signify loss 
of power in individual eye muscles; and while its use in both ways is correct, it is better to 
confine its usage to nuclear and complete lesions. 



PARALYSIS OF EXTRA OCULAR MUSCLES 419 

be fever, vomiting, and even convulsions. Such an attack results 
from minute hemorrhages among the nuclei, or from an acute hemor- 
rhagic polio-encephalitis in the fourth ventricle, arising from syphilis, 
tuberculosis, ptomain poisoning, alcoholic, and sulphuric acid 
poisoning. Such cases are usually rapidly fatal. A less fatal form 
follows injuries, and the effects of nicotine, lead, carbonic oxide, or 
such diseases as diabetes, syphilis, and epidemic influenza. Some- 
times acute ophthalmoplegia comes on with acute poliomyelitis or 
acute bulbar paralysis. 

Chronic nuclear paralysis is gradual in its onset, muscle after 
muscle failing, and even ptosis coming on. Sometimes after a cer- 
tain degree of paralysis is reached the disease comes to a standstill. 
The trouble may be unilateral or bilateral, and is often unsymmetri- 
cal, and it occurs after acute ophthalmoplegia, as a congenital defect 
producing bilateral ptosis (see chapter on the Face), as an acquired 
disease in childhood and adult life, and in conjunction with Locomotor 
ataxia, paretic dementia, disseminated sclerosis, progressive muscular 
atrophy, chronic bulbar paralysis, and in connection with paralysis 
of the frontalis and orbicularis palpebrarum, which are innervated 
by the facial nerve. The cause may be tuberculosis or syphilis, but 
in some cases no cause can be found. 

If the cause of the paralysis of one or two muscles be basilar 
lesions, these may arise from hemorrhage, pachymeningitis, menin- 
gitis, both simple and tuberculous, chiefly the latter; purulent men- 
ingitis, abscess as the result of middle-ear disease, and anemia. It 
may also arise as the result of obliterating arteritis, particularly in 
syphilitics, and from tumors. The frequency with which palsy of 
the ocular muscles depends on syphilis is noteworthy. Alexander 
asserts that 75 per cent, of all cases of unilateral paralysis of the 
third nerve are due to syphilis, and Uhthoff states that only about 15 
per cent, of the cases of cerebral syphilis escape some ocular palsy. 
In children sudden convergent strabismus and diplopia are often 
among the earliest symptoms of tuberculous meningitis at the base 
of the brain due to pressure on the roots of the sixth nerve. 

If the cause be in the nerve trunks themselves, the lesion will 
probably be cellulitis, tenonitis, hemorrhages in the orbit, or frac- 
tures of the orbit; or, again, there may be disease of the frontal 
sinus. If the lesion is distinctly peripheral, it may be due to rheuma- 
tism (when the external rectus is commonly affected), neurasthenia, 
or it may arise from lithemia and gout. Further, such lesions 
may be due to influenza, diabetes, diphtheria, lead, and alcohol, 
or any one of the drugs which paralyze the ocular nerves. 

So much for general statements as to the common and possible 
sites of the lesions producing paralysis of the ocular muscles. 'We 
can now go farther than this, and locate the lesion more accurately 



420 THE EYE 

from the knowledge we have gained as to particular muscles affected 
and the other symptoms presented by the case. 

Let us suppose that a patient suffering from paralytic internal 
squint or a diplopia which indicates paralysis of the external rectus, 
presents himself to the physician, what diagnostic significance has 
this symptom? 1 

In the first place, it is to be remembered that the external rectus 
receives its nerve supply from the abducens, or sixth nerve (Fig. 169), 
which arises from the pyramidal body close to the pons. (See Plate II, 
and Fig. 6.) Its deep origin is a nucleus under the floor of the fourth 
ventricle. The nerve pierces the dura mater on the basilar surface 
of the sphenoid bone (see Plate XV), passes through the clinoid 
process, enters the cavernous sinus, and, finally, enters the orbit 
through the sphenoidal fissure between the heads of the external 




Fig. 169.— Paralysis of left abducens in a case of hemiplegia of syphilitic origin. (Dercum.) 

rectus. If this form of squint is associated with hemiplegia of the 
opposite side of the body, the lesion is in the pons on the same side 
as the affected eye and the opposite from the hemiplegia, because 
the eye fibers have crossed higher up, but the motor tracts for the 
limbs cross lower down. 

On the other hand, if there is monoplegia and abducens palsy 
(internal squint) on the same side of the body, the lesion is in the 
point of origin of the abducens and arm centre in the cortex, or, in 
other words, the lesion has taken place above the point where the 
tracts cross. Such a paralysis is, therefore, cortical. 

If, again, there is complete unilateral paralysis of the abducens 
(internal squint) with loss of the associated action of the internus, 
the lesion is in the nuclei under the floor of the fourth ventricle, 
because the nuclei of the third and sixth cranial nerves are closely 

1 This refers to paralytic and not to concomitant squint. 



PLATE XV. 




iy^^:0- 



Showing the Sixth or Abducens Passing through the Clinoid Process. 
(Modified from Arnold.) 



PARALYSIS OF EXTRA-OCULAR MUSCLES 421 

connected, so that a lesion involving the sixth nucleus weakens the 
nucleus of the third nerve. Complete paralysis of the externus may, 
therefore, be due to a nuclear lesion ; for if the lesion were above the 
nucleus, this nucleus might obtain collateral impulses, and, therefore, 
the paralysis would be only partial. It may also be due to a peri- 
pheral lesion and sometimes an inflammatory process pressing upon 
the basilar surface of the sphenoid, and thereby involving the nerve, 
may cause a similar effect. Loss of power of the external rectus may 
also arise from neurasthenia, gout, and rheumatism, and in tubercu- 
lous or syphilitic meningitis at the; base, as already stated. It also 
comes on in some cases of diabetes, la grippe, and in chronic poison- 
ing by lead and alcohol, or the acute poisoning of gelsemium, 
ptomain poisoning, conium and spigelia poisoning. 

Again, let us suppose that the internal rectus is paralyzed, causing 
external squint. We remember that it is supplied by the oculomotor 
nerve, which springs from the inner side of the cms close to the 
upper border of the pons (see Fig. 8 and Plates I and II ), very near the 
roots of the fourth and sixth nerves. It arises from several roots. 
The nerve itself pierces the dura mater below the posterior clinoid 
process, passes along the outer wall of the cavernous sinus, and after 
dividing into two branches enters the orbit through the sphenoidal 
fissure. (Plates I and XV. ) The upper branch supplies the superior 
rectus and the levator palpebral, and the lower one after dividing into 
three branches supplies the internal rectus, the inferior rectus, and 
the inferior oblique muscles. (See Plate VII.) The oculomotor nerve 
receives filaments from the cavernous plexus of the sympathetic, 
and from the first division of the fifth nerve. In addition to divergent 
squint there are, as already pointed out in the last few pages, in 
oculomotor paralysis, as additional symptoms, ptosis, mydriasis, 
and paralysis of accommodation. 

The lesion producing unilateral ptosis may be found in the cerebral 
cortex on the opposite side from the affected eye in the angular 
gyrus just below the interparietal fissure. Again, tuberculous or 
other degenerative disease of the corpora quadrigemina may cause 
double ptosis. 

If the patient has ptosis with preservation of the function of the 
intraocular muscles (that is, partial oculomotor paralysis), with 
hemiplegia of the opposite side of the body, the lesion, according 
to Mauthner, probably affects the fascicular fibers — that is, those 
between the cortex and the nuclei. There may he associated with 
this form of oculomotor paralysis loss of power in the hypoglossal 
and facial nerves. On the other hand, if the oculomotor paralysis 
is complete, the lesion is almost certainly at the base of the brain, and 
this diagnosis becomes practically certain if there is associated with 
it paralysis of other cranial nerves. Paralysis of the oculomotor 



422 THE EYE 

nerve on one side with hemiplegia on the opposite side of the body 
is not positively a crus or fascicular lesion unless the paralysis occurs 
simultaneously. (Hughlings Jackson.) 

If, however, there be double oculomotor paralysis, the lesion is 
bilateral and probably due to a lesion at the base, as meningitis or 
arteritis (see Plate I), or to an inflammatory exudate involving 
both nuclei; or, again, to diphtheritic poison, or the lesions of tabes 
dorsalis. 

If that very rare form of ocular muscle paralysis, namely, isolated 
palsy of the fourth, or trochlear, nerve, is present, we will probably 
find that the paralysis is due to a lesion at the base of the brain, due 
to meningitis, or the pressure of a growth. 

Supposing, however, that a patient presents himself with swelling 
of the eyelids, exophthalmos, a contracted followed by a dilated 
pupil, anesthesia of the skin of the upper eyelid and of the temple, 
or the area supplied by the first division (ophthalmic) of the fifth 
nerve, and ophthalmoplegia — that is, paralysis of the extrinsic ocular 
muscles on one side — Where will be the lesion productive of this train 
of interesting symptoms ? It will be seen at once that such a con- 
dition is the result of paralysis of the oculomotor (third), pathetic 
(fourth), and abducens (sixth) nerves, and that, as in all proba- 
bility only one lesion has produced these symptoms, it must exist 
at some point where all these nerve fibers are so closely approxi- 
mated that they are readily involved together. It will be recalled 
that the course of these nerves is as follows: the oculomotor nerve, 
having arisen from the nucleus in the corpora quadrigemina, pierces 
the dura mater below the posterior clinoid process, passes along the 
outer wall of the cavernous sinus, and there divides into two branches. 
The pathetic nerve passes near the clinoid process along the outer 
wall of the cavernous sinus, and with the oculomotor nerve enters 
the orbit through the sphenoidal fissure. The sixth nerve pierces 
the dura mater on the basilar surface of the sphenoidal bone, passes 
through the clinoid process, and enters the cavernous sinus, finally 
reaching the orbit through the sphenoidal fissure. It is thus seen 
that a lesion at the sphenoid fissure and pressure in the cavernous 
sinus would cause all the symptoms described above. (See Fig. 170 
and Plates I and XV.) This occurs in cases of thrombosis of the 
cavernous sinus. Where there is an arteriovenous aneurysm of this 
sinus there will be pulsating exophthalmos. Injury or inflamma- 
tion, if in this area, may also produce a series of symptoms. 

The significance of conjugate lateral paralysis producing a devia- 
tion of both eyes to the right or left, as the case may be, is that some 
lesion exists in the cerebral cortex, the corona radiata, or the internal 
capsule, or in the pons before the fibers have crossed. The lesion, 
if in the cortex, however, does not have to be localized in one spot, 



PARALYSIS OF EXTRAOCULAR MUSCLES 



423 



for any source of irritation in the cortex may apparently cause con- 
jugate deviation. If the lesion is the result of an apoplexy, the eyes 




Sphincter irtdis. 
Musculus ciliaris. 
Convergence centre. 
f\ I J Hectus superior. 
S^r.V^^-- Rectus Internns. 

'" levator palpebrae superiorifl. 
- Obliquus inferior. 

- Rectus inferior. 

- Obliquus superior. 



— Rectus externue. 



Fig. 170. — Scheme of the nuclei of the nerves of ocular movement and of their central and 
peripheral tracts: R, right eye: L, left eye; C, chiasm, On, optic nerve; Ot. optic tract; Q, 
pregeminum (anterior quadrigeminal body); P, cortical centre for the movement of elevation 
of the upper eyelid; M, cortical centre for ocular movements; Tn, course of all ocular nerves 
in the cavernous sinus. The names of the different nuclei are printed on the diagram, and 
the nerve tracts going from these nuclei can be readily traced to where they converge in their 
course in the cavernous sinus and where they diverge to pass the various muscles of the eye. 
The dotted lines represent associating and commissural tracts, showing how the fibers of the 
third, fourth, and sixth nerves come together in one bundle in the cavernous sinus. (From 
Mills' Nervous Diseases.) 

are turned toward the side opposite to the paralysis (Prevost's symp- 
tom) — that is, the "patient looks at his lesion." The reason that a 
unilateral lesion can cause a bilateral deviation is that the lateral 



424 



THE EYE 



movements of the eye are governed by an impulse which passes down 
from the cortex to the sixth nerve nucleus, and thence across the 
posterior longitudinal fasciculus to the opposite side, where it passes 
to the nucleus of the third nerve. As conjugate lateral deviation is 
caused by contraction of the internal rectus on one side (third nerve) 
and the external rectus on the other (sixth nerve) the mechanism of 
the deviation is clear. Thus, if the lesion be a distinctive one on the 
left side of the brain, causing right hemiplegia, the eyes will be turned 
to the left by the action of the unaffected left external rectus and the 
right internal rectus; while if the lesion be on the right side of the 
brain, the reverse will occur. If, however, the lesion be irritative 
(as a tumor), this deviation is reversed, because in this case the cen- 
tres are irritated and cause spasm of the muscles receiving their nerve 
supply from the affected side of the cerebrum. In other words, the 
eyes are turned toward the side of the body which is convulsed. 




Fig. 171. — 1. Left ext. rectus. 2. Left int. rectus. 3. Right 
int. rectus. 4. Right ext. rectus. 5. Nucleus left third nerve. 
6. Nucleus right third nerve. 7 and 8. Post, longitudinal 
hands from sixth nerve to opposite third nerve. 9. Nucleus 
left sixth nerve. 10. Nucleus right sixth nerve. 11 and 12. 
Left and right cortical centres. An impulse starting from 12 
would travel down to 9, and produce an associated movement 
of the eyes to the left. 



In the first instance the eyes are turned away from the affected 
side because the muscles of the eyes on that side are also paralyzed, 
and the eyes are, therefore, turned by the muscles which remain 
intact. In the second instance the eyes are turned toward the con- 
vulsed side because the internal and external rectus are spasmodi- 
cally contracted and so overcome the healthy muscles. 

We find, however, that if the lesion be in the pons rather than in 
the cortex, these conditions are reversed, for now a destructive 
lesion causes the eyes to be turned to the paralyzed side, and an 
irritative lesion directs them away from the paralyzed side. 

This is best explained by the following diagram and description 
from Swanzy's well-known book (Fig. 171). 

A destructive lesion at twelve, the right cortical centre, involving 
also motor centres of the body, would cause left hemiplegia; and, 
since the external rectus of the left eye and internal rectus of the 
right eye would be paralyzed, the antagonists would turn the eyes to 
the right— i. e., away from the paralyzed side. A destructive lesion 



PARALYSIS OR DISORDER OF INTRA OCULAR MUSCLES 125 

of the right side of the pons, also producing left hemiplegia, if it 
involves the sixth nucleus, will produce paralysis of the external 
reel us of the right eve and of the internal rectus of the left eye, and 
then the antagonists would turn the eyes to the left — i. e. s toward 
the paralyzed side. It is easy to see how irritative Lesions would 
produce exactly the opposite effects. 

Squint which is due to hysteria is always caused by spasmodic 
contraction of the eye muscle and is never due to paralysis, as it 
often is in organic disease. Very often there is a spasm of the eyelid 
or eyebrow associated with it. The administration of a relaxant, 
such as chloroform, will at once overcome such a squint. 

Nystagmus, or the rapid oscillation of the eyes from side to side 
or in a vertical or rotary movement, i- usually bilateral. 1 When not 
congenital it is a frequent symptom of disseminated sclerosis, 
Friedreich's ataxia, and advanced locomotor ataxia; and while it 
• Iocs not localize the lesion, it indicates very positively that one is 
present and that the case is not one of hysteria or functional disease. 
Nystagmus occurring in children i^ very often associated with imper- 
fect vision of great degree or with blindness as a result of opacity 
of the cornea, congenital cataract, or atrophy of the nerve. In other 
instances, however, it arises from growths in the cerebellum or pons, 
and it is sometimes seen in hydrocephalus and Aery rarely in acute 
meningitis and in epilepsy. Very rarely lateral nystagmus is seen 
in children who seem otherwise normal, and it then possesses no 
particular diagnostic importance. 

Paralysis or Disorder of the Intra-ocular Muscles. — Having dis- 
cussed the diagnostic indications of changes in the functions of the 
extra -ocular muscles, we next proceed to a consideration of these 
facts in connection with the intra-ocular muscles. These consist, it 
will he remembered, in the muscular fibers of the iris, circular, and 
radiating, and the ciliary muscle. The nerve supply of the iris con- 
sists in fibers from the oculomotor or third nerve, the upper or 
ophthalmic division of the fifth, and the sympathetic. It will be 
remembered that in the posterior part of the orbit there is situated a 
ganglion called the ciliary or ophthalmic ganglion. By its short or 
motor root this ganglion is connected with the third nerve, bv its 
sympathetic root with the cavernous sympathetic plexus and the 
cervical sympathetic plexus, while by its long or sensory root it is 
connected with the nasal branch of the ophthalmic or upper branch 
of the fifth nerve. From this ganglion extend forward two sets of 
nerves, one short ithe short ciliary nerve), which supplies the iris 
and the ciliary muscle, and one set long ^long ciliary nerves), which 
also go to the iris. The filaments which go to the ganglion by means 

!The physician should remember that some occupations, such as mining, produce in some 
persons nystagmus without the presence of the disease about to be named. 



426 THE EYE 

of its short or motor root (from the oculomotor nerve) pass forward to 
the circular fibers of the iris, while those which have arisen in the 
sympathetic plexus pass forward to the radiating fibers. These last 
fibers are in part derived from the cervical sympathetic ganglion, 
run through the carotid plexus, and are controlled to some extent by 
the ciliospinal centre of Bunge in the spinal cord at about the seventh 
cervical or first dorsal vertebra. 

The ciliary muscle is supplied by the fibers of the short ciliary 
nerves, which have arisen in the floor of the third ventricle and which 
is connected with the nucleus of the third nerve. 

Testing the Pupil. — The normal pupil is about 4 mm. in diam- 
eter, but this varies according to the degree of light to which the 
patient is exposed. It ought always to be measured by a millimeter 
measure, which gives its approximate diameter. 

The pupil to be tested must be free from any abnormal conditions 
produced by new or old inflammation of the iris, and the light used 
should not be excessively bright, but about that usual to the eye. 

The patient is to be placed facing the light and told to look at 
some distant object. The hands of the physician are then placed 
one over each eye, the patient being told to keep his eyes open. 
One hand is now quickly removed from one eye and the pupil 
observed. This observation must be acute or the pupillary contrac- 
tion will occur before it is seen. This reflex is due to the fact that 
we have an irritation of the optic nerve by light, and this sends a 
reflex wave to the centres governing the pupil and causes it to con- 
tract. Not only does the uncovered pupil react in this manner, but 
the covered one does the same thing. The first is called a direct 
reflex, the second is called the indirect or consensual reflex. The 
exact pathway of this reflex is unknown. 

Not only does the pupil change its size by reason of the ordinary 
light reflex, but it also contracts or dilates in association with the 
other muscles governing accommodation and convergence, namely, 
the ciliary muscle and internal recti. This is the associated reaction 
of the pupils, and is tested by causing the patient to direct his eyes 
to a near object — for example, the point of a pencil. If the sight 
is intact, contraction of the pupil will occur. 

The pupil-dilating centre is in the medulla and is very sensitive 
to reflex irritation. 

Abnormal Pupillary Movement. — Supposing that the pupillary 
movement is abnormal, we should recollect before studying the 
case farther what the causes of its perversion may be. Thus, its 
size is altered by drugs, by local disease of the iris, by spinal dis- 
ease of the sympathetic, by localized cerebral lesions, by abeyance 
of the cerebral functions, and by irritation of the brain. Let us 
suppose, however, that on testing the ocular reflexes in the manner 



ABNORMAL PUPILLARY MOVEMENT 427 

already described we find that the pupil of one eye when uncovered 
does not contract, and immediately does so as soon as the other eye 
is uncovered, What is the indication? It indicates that there is 
disease of the optic nerve of that eye which does not convey the 
impulse of light from the retina; whereas, if it contracts when the 
other eye is uncovered, it shows that the rest of the mechanism 
involved in the reflex is intact. Accommodative reaction of the 
pupil is intact also. 

If the irides fail to react to light, but do to accommodation and 
convergence, we have the "Argyll-Robertson pupil," so called, 
which indicates that a lesion exists in the fibers back of those 
concerned with the ordinary light reflex. 

This condition is seen in locomotor ataxia, general paralysis 
of the insane, sometimes in cerebral syphilis, and as the result of 
poisoning by the bisulphide of carbon. Grube has reported three 
cases in which the Argyll-Robertson pupil developed in the course 
of diabetes mellitus. Marinesco has reported an instance of Argyll- 
Robertson pupil in a patient suffering from amyotrophic lateral 
sclerosis. It is worthy of note, however, that late in all these affec- 
tions the reaction to accommodation may also be lost. Rarely the 
reverse of the Argyll-Robertson pupil occurs as the result of a lesion 
in the second and third parts of the oculomotor nucleus. If the eyes 
fail to react to light and to accommodation, there is probably blind- 
ness due to optic-nerve disease. 

If on throwing light into the right eye there is no reaction of the 
pupil of that eye, and on throwing it into the left eye there is still 
no reaction in the pupil of the right eye, there must be a lesion of 
the nucleus of the right oculomotor nerve or palsy of the conducting 
fibers of each optic nerve. 

Sachs asserts that immobility of the pupil is very characteristic 
of syphilitic cerebrospinal disease, and if the diagnosis lies between 
multiple sclerosis on the one hand, and cerebrospinal syphilis on 
the other, the discovery of immobility of one or both pupils should 
decide in favor of its being a syphilitic case. He also asserts that 
persistent pupillary immobility in a case of hemiplegia indicates a 
syphilitic endarteritis. It is important in this connection to remem- 
ber that the pupillary changes due to syphilis often suddenly improve, 
while those due to sclerosis are absolutely permanent. 

Contraction of the pupil occurs in a large number of conditions 
and yet possesses considerable diagnostic significance. Thus it is 
generally found in the early stages of all acute inflammatory pro- 
cesses in the brain or its membranes. In cerebral hemorrhage it is 
usually contracted at first, thus serving to separate acute paralysis 
due to hemorrhage from that due to embolism, for in the latter 
Berthold states that the pupil is unaltered. In the early stages of 



42S THE EYE 

intracranial tumors which irritate the third-nerve nucleus it is also 
contracted. Finally, we find myosis as a result of chronic tobacco 
poisoning, from irritation of the pupil-contracting centre by nicotine, 
at the beginning of an attack of hysteria or epilepsy, and in watch- 
makers and jewellers. Such forms of myosis are called "irritative 
myosis." Myosis is also seen in disease of the apex of the lung. (See 
next page.) 

Paralytic myosis is met with in lesions above the dorsal vertebra 
of a chronic type, as a rule. Its most interesting form is that seen 
in locomotor ataxia, when the disease has involved the ciliospinal 
centre. 

Of course, pupillary contraction may result from the action of a 
myotic drug, as eserine or pilocarpine. 

Dilatation of the pupil may also be due to irritation or paralysis. 
Thus, irritation of the pupil-dilating centre may cause mydriasis, 
and this is met with in congestion of the cervical spinal cord and in 
spinal meningitis, as the result of tumors in the cervical cord, in 
spinal irritation, in the anemia of convalescence, as an early sign of 
tabes dorsalis, and in acute mania. Certain cases of acute croupous 
pneumonia present dilatation of both pupils, the dilatation being 
most marked on the affected side, probably by irritation of the sym- 
pathetic fibers by pressure of the consolidated lung. Sometimes in 
progressive paralysis of the insane there may be irritative mydriasis 
in one eye and myosis in the other. Von Graefe asserted that alter- 
nating unilateral mydriasis is an early sign of mental derangement. 

The states in which we find paralytic mydriasis are in the later 
stages of progressive paralysis, in lesions at the base affecting the 
oculomotor centre, late in thrombosis of the cavernous sinus, in orbital 
disease which causes pressure on the ciliary nerves, in glaucoma, 
and in intracranial growths of considerable size. Not only may 
paralytic mydriasis be due to an oculomotor lesion, but as the result 
of some blocking of the pathway from the retina to the centre. 1 

Under the name of (( hemiopic pupillary inaction" or " Wernicke's 
pupil/' we sometimes, though rarely, meet with a condition asso- 
ciated with hemianopsia, or blindness in one-half of the eye, which 
is demonstrated in the following manner: the patient is seated in a 
dark room and one eye is covered. The other eye is now illuminated 
by just sufficient light from a flat mirror to enable the physician to 
see the eye. By means of the concave mirror of an ophthalmoscope 
the physician now directs into the uncovered eye a bright beam of 
light, taking care that it falls upon one side of the retina, or, in other 
words, enters the eye obliquely and strikes on the side of the retina 
which is blind. If when the light falls on the blind side of the retina 

i For a useful summary of these facts and for references, see "Diseases of the Eye," by 
Svvanzy, sixth edition. 



CHANGES IN THE ACUITY OF VISION |29 

there is no pupillary reaction, it is considered that the lesion exists 
in the arc between the optic chiasm and the corpora quadrigemina; 
bill if there is a pupillary reaction, the lesion must be farther back 
in the visual centres, hack of the reflex arc. When the lesion is found 
back of the reflex arc it may indicate a lesion of the optic tract, the 
posterior segment of the thalamus, the posterior part of the chiasm, 
or rarely it may be caused by a lesion of the optic nerve if the hemi- 
anopsia be monocular, which is rarely the case. 

Finally, a rhythmical contraction and dilatation of the pupil, 
called ' hippus" is seen in health for a moment on sudden exposure 
to light; but when constant is a sign of disseminated sclerosis, 
epilepsy, or the early stages of acute meningitis. It is sometimes 
seen in hysteria. 

The presence of a recurrent, unequal dilatation of the pupils of 
a transitory character is said by Rampoldi to be an early and almost 
constant sign of pulmonary tuberculosis. He believes that this is 
due to a reflex irritation of the nerves governing the pupil through the 
sympathetic system. Probably in these cases enlarged glands in the 
chest are the cause of the pupillary phenomenon. Destree claims 
that 97 per cent, of his cases of phthisis present this pupillary symp- 
tom. On the other hand Souques asserts that myosis is commonly 
present in tuberculous apical disease owing to the dilator fibers from 
the ciliospinal centre which pass through the first dorsal nerve to the 
cervical sympathetic being pressed upon by the apex of the pleura. 
Evidently it is an irritative reflex and results in mydriasis or myosis 
according to the degree of pressure. 

Knies points out that pupillary contraction and dilatation take 
place in association with Cheyne-Stokes breathing. Dilatation 
usually exists with the inspiratory movements, and myosis occurs 
during the interval of apnea. 

Changes in the Acuity of Vision. — Having discussed the diag- 
nostic value of alterations from the normal in the function of the 
extra- and intra-ocular muscles of the eye, we can proceed to a con- 
sideration of the value of changes in the acuity of vision. The ques- 
tions of the acuity of vision in relation to errors in the refractive 
media of the eye will not, of course, be included in this book. 

Failure of vision in part or in toto depends upon a lesion which 
destroys the peripheral ocular sense organ (the eye), the optic nerves, 
the optic tracts, or the receptive and perceptive centres of sight. It 
also is dependent upon bilateral lesions in the crystalline lens, as in 
cataract, or in the cornea, as in severe keratitis. 

Before we discuss these various causes of blindness it is necessary 
that we recall the nervous anatomy of the organs of sight. These 
nerve fibers starting with the rods and cones of the retina and the 
fibers from the macula pass back along the optic nerve until they 



430 



THE EYE 



come to what is known as the chiasm, where the various fibers from 
the eye decussate, in that the fibers from the inner half of each eye 



teft Ey, 



VtinialFVelcZ 




Fig. 172. — The visual tract. The result of a lesion anywhere between the chiasm and the 
cuneus is to produce homonymous hemianopsia. H. Lesion at chiasm causing bilateral tem- 
poral hemianopsia. N. Lesion at chiasm causing unilateral nasal hemianopsia. T. Lesion 
at chiasm causing unilateral temporal hemianopsia. SN. Substantia nigra of crus. L. Lem- 
niscus in crus. RN. Red nucleus. III. Third nerves. P, Q, R, S, U Lesions in the occipital 
lobe and in front of it, producing left homonymous lateral hemianopsia. 



CHANGES IN THE ACUITY OF VISION 



431 



cross to the opposite side, whereas those of the outer half of each 
pass to the same side, as is shown in Fig. 172. After the optic tracts 
have been formed by this (partial) decussation each one winds 
around the corresponding cms cerebri, and terminates in two roots 
upon the corpora geniculata externa and interna and upon the pos- 
terior part of the optic thalamus. These parts are known as the 
primary optic centres. After leaving them the fibers pass backward 
into the posterior part of the posterior limb of the internal capsule 
and thence to the cortex, rise in a fan shape, pass outside the tip 
of the lateral ventricle, and reach the secondary or true optical 
centre in the lower part of the median aspect of the occipital lobe 
(Fig. 172). 

LEFT VISUAL FIELD. RIGHT VISUAL FIELD. 
Fixation Point. Fixation Point . 




Fig. 1 



(Oliver.) 



Hemianopsia. — As lesions of the nervous centres frequently produce 
partial or complete blindness, it is of importance, first, that the pres- 
ence of partial blindness should be discovered, and, second, that 
the lesion causing it should be located. Aside from general failure 
of vision due to changes in the retina or optic nerve we have in many 
cases of nervous disease a condition called hemianopsia or partial or 
complete blindness of one-half of the retina. Usually hemianopsia 
is bilateral — that is, in both eyes; and it is usually homonymous — 
that is, on the same side of each eye; or, in other words, if it is in the 



432 



THE EYE 



outer half of the left eye, it will be in the inner half of the right eye. 
If this is the case, it is called left bilateral homonymous hemianopsia. 
If, on the other hand, the outer half of each eye is blind, this is called 
bitemporal hemianopsia; if the blindness is found in the nasal side 
of both eyes, it is called binasal hemianopsia. It must be remem- 
bered, however, that the apparent blindness of the outer side of the 
eye is really due to disease of the fibers supplying the opposite side 
of the retina, as is shown in Fig. 173. 

The presence of hemianopsia in any form is determined by the 
following method of examination: The patient is placed with the 




Fig. 174. — Chart of visual field of right eye. 

back to the light and one eye is covered while the other is fixed upon 
the centre of the physician's face, which should be two feet away. 
The finger of the physician is now moved to the left and right as far 
as the patient can see it, the head and the eyeball of the patient 
remaining fixed. If the eye fails to see the finger when but a little 
distance to one side or the other of the fixation point, hemianopsia 
is present. 

We measure the field of vision more accurately by means of what 
is known as a perimeter, which is a semicircular metal band which 
revolves upon its middle point, being capable therefore of describing 
a hemisphere in space. This arc is divided into degrees marked on 



CHANGES IN THE ACUITY OF VISION 



433 



from 0° to 90° and at the centre of it is placed the eve which is to be 
cammed, which eve finds its fixation point in the centre of the scmi- 
ircle. A small piece of white paper is now moved along the metal 




Fig. 175. — Left homonymous hemianopsia from a case of gunshot wound, with suspected 
lesion of the right cuneus. (de Sehweinitz.) 

arc on its inner surface, from the extremity and toward the centre, 
until it comes into view, when the physician notes the number 
of degrees at which the object is seen and marks it on a chart 
(Fig. 174). The area of the normal held is well seen in this figure. 




160 360 



210 330 




so 



270 270 

Fig. 176.— Bitemporal hemianopsia from a case of acromegaly, (de Sehweinitz.) 

Let us suppose that on using the tests just described we find left 
lateral homonymous hemianopsia — that is, blindness in the visual 
field, as shown in Fig. 175. This signifies that the patient has a. 

2S 



434 



THE EYE 



lesion somewhere in the visual tract back of the chiasm, either in the 
cuneus, in the occipital lobe, in the optic radiations, in the internal 
capsule, in the primary optic centres, or in the optic tract. Fig. 172 
shows the sites of these lesions and why they cause left homony- 
mous hemianopsia. 

Supposing, on the other hand, that instead of left homonymous 
hemianopsia we find bitemporal hemianopsia (Fig. 176), this indicates 
that the patient has a lesion of the optic tracts in the crossing 
fibers in the middle of the chiasm (see H in Fig. 172); or if binasal 




WHITE 

BLUE 

RED 

GREEN 

Fig. 177.— Chart of visual field of left eye. (Landolt.) 

hemianopsia, that he has a lesion on both sides of the chiasm or one 
on the outer side of each optic nerve. This is a very rare lesion. 

Hemianopsia of the homonymous form is very rarely found in 
hysteria, generally in association with hysterical hemianesthesia, in 
which condition the conjunctiva is usually anesthetic, thereby differ- 
ing from the condition of the conjunctiva of persons suffering from 
hemianesthesia of an organic origin. 

Visual Color Fields. — In some cases in place of hemianopsia we 
have simply an alteration in the visual fields for color. It will be 
remembered that the boundaries of the power of the clear perception 
of colors are not identical with the boundary for white light, nor are 



CHANGES IN THE ACUITY OF VISION 



435 



they identical with one another. Passing from the periphery toward 
the centre of the visual field in ordinary daylight we find that blue is 
the color first seen, its boundary being almost as great as that of 
white. After blue come yellow, orange, red, and finally green. The 
blue, red, and green being the most important colors, their bound- 
aries are shown in Fig. 177. These fields are determined by means 
of small pieces of colored paper passed around the perimeter in 
the manner already described. 

The alteration of the visual field for colors is called, if so changed, 
homonymous hemidy schromatopsia, and the lesion producing it is 
situated in the cortex of the occipital lobe; while if the colors are 
indistinguishable, it is called hemiachromatopsia. r i This site of the 
lesion has recently been denied. 

The transposition of the visual fields for color is usually a symp 
torn of hysteria, and, as a rule, the red field takes the place of the 
blue, and vice versa. The fields for all the colors are also markedly 
narrowed in hysteria. This transposition, rather than loss of color 
sense, helps us sometimes to a distinction between tin' ocular symp- 
toms of hysteria and those of true tabes dorsalis, a distinction which 
is of great importance, yet one which is often exceedingly difficult, 
save for these and two other symptoms, namely, that in hysteria 
the knee-jerks are usually preserved and the Argyll-Robertson 
pupil is not seen. The following table from Charcot's lectures for 
1888-1889 summarizes these differential points: 





Tabes. 


Hysteria. 


Motor apparatus of the 


Paralysis from lesion of a motor 


1 


Sometimes associated paralysis. 


eye. 


nerve of the eye (bulbar or per- 


o 


Blepharospasm. 




ipheral) ; consequent diplopia. 


3. 


Monocular diplopia ; micropsia 
and macropsia. 


Pupillary disturbances. 


Argyll-Robertson pupil. 






Optic disk. 


Atrophy. 






Symptoms due to affec- 


1. Irregular concentric contrac- 


1. 


Regular concentric contraction 


tions of the optic uerve 


tion of the visual fields. 




of the visual fields. 


or visual centres. 


2. Tabetic achromatopsia or dys- 


g 


Dyschromatopsia from simple 




chromatopsia, affecting first 




contraction of the visual fields 




green and red, yellow and blue 




for colors. Frequently percep- 




being preserved to the last. 




tion of red alone persists. 




3. Progressive blindness. 


3. 


Transitory amblyopia or amau- 
rosis. 



It must not be forgotten that patients often have, in distinction 
from distorted images, visions or flames of light or bright sparks 
before the eyes, or in their place dark spots called muscae volitantes. 
Often the visions are the prodromes of an attack of migraine or of 
an epileptic seizure. In the case of spots of light or stars we usually 



436 THE EYE 

find them as a result of severe indigestion, and the dark spots may 
arise from the same causes. Muscce volitantes may also be due to 
small particles of mucus floating over the cornea or to small floating 
bodies in the vitreous. 

Partial or complete blindness is sometimes seen in cases which are 
under the influence of a drug, as, for example, quinine or other drugs; 
and sometimes partial or complete blindness results from uremia 
(uremic amaurosis). As a rule, it does not occur as a single symptom, 
but follows an attack of acute uremic manifestation — that is, it is 
found after a convulsion or period of coma has passed by. As a rule, 
nothing abnormal is found in the eye to account for it, and the pupil- 
lary reflexes are intact. The effect of the poison in the blood is, 
therefore, exercised upon the optical centres, probably in the occipital 
lobe. Sight is usually regained in these cases in a few days. 

The Optic Nerve and the Ophthalmoscope. — There still remain 
to be considered the diagnostic indications afforded us by the optic 
nerve. Before taking up this subject mention must be made of the 
manner of using the ophthalmoscope. 

The patient is to be seated in a darkened room, and by his side, 
at the level of the eye to be examined and far enough back of him 
for his face to be in shadow, should be placed a lamp, or, if gas can 
be had, an Argand burner. The physician now seats himself, if 
the right eye is to be observed, at the right side of his patient, and takes 
a chair slightly higher than that of the patient. The ophthalmoscope 
is now taken in the right hand and held in such a position that the 
concavity of the physician's brow fits over the convexity of the instru- 
ment. The eye of the physician is so placed that he can readily see 
through the aperture in the centre of the ophthalmoscope, and by 
means of the concave mirror on the face of the instrument he reflects 
the light into the eye through the pupil. The patient must not look 
into the ophthalmoscope, but to one side, and his vision should be 
directly distant and accommodation as far as possible relaxed. If the 
examiner is not skilled in the use of the ophthalmoscope and the 
result of the examination is of great importance in the diagnosis of the 
case, it is justifiable to use homatropine to dilate the pupil and 
prevent the alterations of accommodation by paralyzing this func- 
tion. The ophthalmoscope and the head of the physician are now 
approached as closely as possible to the eye of the patient, the angle 
of the two heads being as nearly as possible identical, as shown in 
Fig. 178. If the light be now directed slightly toward the nasal side 
of the eye, the optic nerve will be seen, or in its stead a retinal blood- 
vessel will be seen across the field of vision, and this should be traced 
along its course to its origin in the papilla. If the patient or the 
physician is short-sighted (myopic), the ophthalmoscope must be 
adjusted to correct this error by placing over the aperture a concave 



77/ A' OPTIC NERVE AND THE OPHTHALMOSCOPE 



437 



lens; hut if ordinary degrees of far-sightedness (hypermetropia) are 
present, the use of a convex lens is riot necessary, because the accom- 
modation of the eye makes up for the error in refraction. If the 
hypermetropia is so great that accommodation eannot overcome it, 
then a convex lens must he used. The view of the eye which is 
obtained ordinarily by a beginner is clouded, not because of myopia 
or hypermetropia, but because the physician has not as yet learned to 
relax his accommodation in making the examination. A concave 
glass usually remedies this. 




Fra. 178. — Relative position of physician and patient whilst employing the direct method. 

(Norris and Oliver.) 



In health the optic nerve appears as a nearly round or slightly 
oval disk, situated somewhat to the nasal side of the eve, and varying 
in color from grayish pink to red, the centre being whiter and the 
nasal half the darkest part. Around the papilla are seen two rings, 
the outer one darker and generally incomplete or absent, while the 
inner one is. a faint white stripe, which becomes more marked as 
the patient grows older. The first is called choroidal ring, and repre- 
sents the C(]ge of the choroidal coat of the eye where it is pierced by 
the nerve. The second is the scleral ring, which is the edge of the 



438 THE EYE 

sclerotic coat. The centre of the optic papilla may be even with the 
surface or cupped, and may be stippled or dotted in appearance. 
The retinal arteries emerge from this central spot and the chief 
venous trunks empty into it. Generally one arterial and one venous 
stream pass up and a similar one downward, and both soon bifurcate, 
afterward still further dividing. The arteries are distinguished from 
the veins by their bright-red hue, while the veins are darker in color. 
The veins are about one-third larger than the arteries. A bright 
stripe due to an optical delusion seems to divide each vessel longi- 
tudinally into two parts. The arteries of the normal eye do not pul- 
sate, but pulsation of the veins is quite common. It must be remem- 
bered that the appearance of the papilla and of the bloodvessels as 
they leave it varies very greatly within perfectly physiological limits. 
As already stated, the cupping of the papilla may be quite deep or 
quite shallow, and the bloodvessels may divide as already described, 
or divide in the papilla into four branches. The veins are usually 
more tortuous than the arteries. The retina is practically trans- 
parent, so that the underlying choroid is seen. In persons with a dark 
skin the retina has a grayish hue in the neighborhood of the papilla, 
which is most marked on its nasal side and is slightly streaked. 

To the outer side of the papilla, slightly below the horizontal 
meridian, is the macula lutea or yellow spot, which is about the size 
of the end of the optic nerve, but darker in color, somewhat granular, 
and devoid of any retinal vessel. It is the point of the eye-ground in 
which direct vision is best developed. In its centre is a bright spot, 
the fovea centralis. As a person grows older these clear distinctions 
vanish and the macula lutea is to be distinguished from the surround- 
ing eye-ground only by its darker hue and the absence of vessels. The 
macula is difficult to see, because as the light falls on it the pupil at 
once contracts. If the eye is dilated by a mydriatic, however, and 
the patient looks directly into the ophthalmoscope, the macula is 
readily seen. 

The red glare produced by throwing the light into the eye by the 
ophthalmoscope is due to reflection from the bloodvessels of the 
choroid coat. 

The pathological significance of alterations in these normal appear- 
ances is very great. 

Optic Neuritis. — Let us suppose that on examining the eye- 
ground we find the end of the optic nerve red and its edges irregular 
and obscure, or, if the morbid condition is further advanced, that the 
nerve head looks protruding or mound-like and the arteries going 
to it are smaller than normal and partly concealed, while the veins 
are enlarged and tortuous. Hemorrhages may be seen in the papil- 
lary region or near it, occurring in flame-like shapes. These are the 
signs of optic neuritis, and optic neuritis depends upon intra-orbital 



THE OPTIC SERVE AXD THE OPHTHALMOSCOPE 439 

or intracranial disease, although, if the process is not marked, it may 
be due to hypermetropic astigmatism. Vision is often unaffected, 
but if the lesion be in the cerebellum sudden blindness may come on. 
As some differences of opinion exist as to the various forms of 
neuritis of the optic nerve, the term papillitis is often used to signify 
all the forms of optic neuritis which we meet with, or in other cases 
is spoken of as "choked disk." Papillitis is more commonly the result 
of brain tumor than of any other intracranial lesion, and, again, 
it is much more common in lesions of the cerebellum than in tumors 
elsewhere in the brain. Another fairly common cause of papillitis 





























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15 - 20 


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26-30 


31-35 


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41-45 


46 - 50 


51 - SS 


56 - 60 


61-65 


66-70 


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Fig. 179. 



•Upper curve, frequency of tabes. Middle curve, frequency of severe ocular symp- 
toms. Lower curve, frequency of atrophy of the optic nerve. (Berger.) 



is meningeal inflammation, particularly about the base of the brain, 
and tuberculous meningitis is very prone to produce it. Cerebral 
abscess may also cause this change in the optic nerve. 

In addition to the cranial causes of papillitis we have acute febrile 
disorders, syphilis, toxemias from lead and alcohol, rheumatism, and 
anemia. Sometimes, however, they produce an acute or chronic 
retrobulbar neuritis. There is nearlv always in such cases a large 
central scotoma, which causes a failure to recognize color, as, for 
example, green or red. Sometimes the patient realizes the failure of 
his vision, which may be impaired otherwise than by disorder of 
the color sense. In other cases he fails to do so until his eves are 



440 THE EYE 

examined. The chronic form of retrobulbar neuritis is generally 
the result of the excessive use of tobacco and alcohol, and produces 
what is called tobacco amblyopia or toxic amblyopia, with failure of 
vision from these causes. In such cases there is a central scotoma 
between the macula and the optic nerve where the senses of red 
and green are lost. The ophthalmoscope may reveal in such cases 
discoloration of the disk and a triangular spot of atrophy in.the outer 
and lower part of it. Supposing, however, on using the ophthalmo- 
scope we find in place of a papillitis an atrophied state of the nerve, 
in which, if the disease be young, the nerve ending looks gray and 
the outline of the disk is sharp, or if it be well advanced the edges 
appear hazy, the arteries contracted, and the veins large and tortuous, 
while the disk is quite white. This primary or gray form of atrophy 
is most typically seen in the optic-nerve lesion of locomotor ataxia, 
and so is often called tabetic atrophy. About 34 per cent, of all 
tabetics suffer from this change. Again, it is seen in cases of paretic 
dementia somewhat less frequently. Optic atrophy is often seen in 
cases of disseminated sclerosis. Because of the fact that gray atrophy 
of the nerve is one of the earliest signs of locomotor ataxia, in some 
cases it is a valuable one in the diagnosis of this grave disorder, 
separating it from pseudotabes due to ordinary peripheral neuritis. 
The diagram (Fig. 179) on page 439, taken from de Schweinitz's 
article on this subject, shows the relation between age, severe ocular 
symptoms, and atrophy of the optic nerve. 

The more advanced forms of optic atrophy with a hazy outline of 
the disk usually result from diseases in the optic centres or in the 
nerve itself. Thus there may be present a tumor pressing on the 
chiasm or optic tracts. 

Retinitis. — If on the use of the ophthalmoscope we find that there 
is a faint haziness of the retina, that whitish streaks are seen in it 
which may be bluish-gray or yellowish in hue, that the bloodvessels 
are tortuous and minute vessels are easily seen because of their 
enlargement, that hemorrhagic exudations of a flame-like character 
are present, that dark pigmented spots show where previous hem- 
orrhages have been, and, finally, that the head of the optic nerve 
is not clearly outlined, we have the picture of retinitis. Generally, 
in association with these signs, we find as subjective symptoms 
changes in the visual field, a distorted vision, so that straight lines 
appear bent inward or outward, and there are pain and fear of light. 
If in addition to these symptoms the vitreous humor is opaque, 
syphilis may be present, and the iris may give evidence of iritis. 
Where the hemorrhages are very manifest and profuse (hemorrhagic 
retinitis) the cause may be disease of the heart and bloodvessels. 

By far the most important of these forms of retinitis from a diag- 
nostic standpoint is what is known as albuminuric retinitis, or that 



THE OPTIC NERVE AXD THE OPHTHALMOSCOPE 44 1 

due to parenchymatous nephritis. Here, in addition to the flame-like 
hemorrhagic areas, we find irregular spatterings of white which may 
be star-shaped. If the retinitis be due to chronic Bright's disease the 
prognosis is very had, death occurring in a year in .")() per cent, of 
the eases, whereas not 20 per cent, live more than two years. The 
importance of the discovery of such changes is that by it the first 
suspicion of renal trouble is aroused. This sign is of the greatc-t 
value in pregnancy, in which the ultimate prognosis is not so grave. 
Retinitis also sometimes results from diabetes. 

Hemorrhages into the retina without retinitis are usually the result 
of septicemia, ulcerative endocarditis, hemophilia, diabetes, gout, 
and malarial fever of a severe type, They are also seen in cases of 
great cardiac hypertrophy with stenosis, and after suffocation. 

Ophthalmoscopic evidence of general arterial disease and chronic 
contracted kidney not infrequently is manifested by edema of 
the retina and retinal hemorrhages; hut an early sign is the 
influence of the arterial pressure on the venous blood streams 
of the retina, where artery and vein cross one another. There 
may be simply inequality in the caliber of artery and vein, or 
the vein may be somewhat displaced, where it lies beneath 
the artery, in the direction of the arterial circulation, and it> 
flow obstructed. In advanced cases the vein is greatly narrowed 
where the artery crosses it and distended on its peripheral side. 
When these appearances are well studied they are exceedingly sug- 
gestive of early arterial changes. Changes of this character, as the 

D • DO 

author can testify from studies made 1 with \)y. de Schweinitz, are of 
serious prognostic import and may be the forerunners of intracranial 
extravasations. 

Iris. — The iris indicates disease in other organs more rarely than 
the retina and optic nerve and the muscles, but an irregular pupil 
indicating an old iritis should raise a question as to a history of injury 
or rheumatism or syphilis. 

Finally, it should not be forgotten that cataract sometimes occurs 
as the result of diabetes mellitus and that corneal ulceration is often 
an evidence of scrofulous tendencies, while a distorted pupil due to 
an old iris should raise a suspicion of syphilis. 



CHAPTEE XIV. 

CHILLS, FEVER, AND SUBNORMAL TEMPERATURES. 

Chills— The methods of taking the temperature — The significance of fever — 
The febrile movements of various diseases. 



CHILL. 



A chill is of very considerable diagnostic importance when 
observed by the physician, or even when reported as having occurred 
in the immediate history of the patient. It may follow prolonged 
exposure to cold, without subsequent development of disease, or be a 
precursor of some acute malady. Often it is an early symptom of the 
onset of one of the acute infectious diseases, such as croupous pneu- 
monia, erysipelas, or scarlet fever. In other instances it is a symptom 
of the development of a purulent or pyemic process. When chills 
recur repeatedly they may be due to malarial infection, in which case 
they may be controlled by using quinine; as a result of deep-seated 
abscesses and general pyemia ; and finally, they may indicate tuber- 
culosis or ulcerative endocarditis. In some cases of typhoid fever a 
chill ushers in the attack, and chills may repeatedly occur without 
apparent cause, so that the disease may be singularly like remittent 
malarial fever. (See Figs. 180 and 181.) 



FEVER. 

Fever is that state of the human body in which its temperature 
is raised above the normal limit, or 98.8° F., but variations from 
97.8° to 99.5° may occur without indicating disease. From 99.5° to 
100.4° the temperature is spoken of as subfebrile, from 100.4° to 
101.3° as mildly febrile, while the term decidedly febrile is applied to 
temperatures varying from 103.1° to 105°. Hyperpyrexia is a term 
applied to a febrile movement in which the temperature rises as 
high as 106°. Cases are on record of a temperature of 115° or even 
more. 

The method of taking the temperature consists in placing a self- 
registering clinical thermometer in the mouth under the edge of the 
tongue, the lips being then closed tightly about its stem; or of insert- 
ing it in the axilla, the hand and arm being then placed across the 






FEVER 



443 



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Fig. 180. — Toward the end of this case of typhoid fever severe chills developed on the 
eighteenth, nineteenth, and twentieth days, and the fever ended by crisis. 



444 CHILLS, FEVER, AND SUBNORMAL TEMPERATURES 

patient's chest or epigastrium, so as to cause the axillary tissues to 
be in close contact with the bulb of the thermometer. Before the 
thermometer is placed in the axilla this space should be carefully 
wiped dry, since if perspiration is present its evaporation will so 
chill the thermometer that a false record will be made by the index. 
Sometimes the temperature of the patient is taken by inserting the 
thermometer into the rectum; and, if this is done, the bulb should 
be passed well inside the external sphincter. Rarely the temperature 
is taken in the vagina. In the rectum and vagina the normal tempera- 



BOWELS 
MOVEMENTS 


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Fig. 181. — " Chills and fever " in course of typhoid fever. 

ture is about one to one and a half degrees higher than in the axilla. 
In fat children the fold in the groin gives equally reliable results 
with those obtained by inserting the thermometer in the rectum. 

The precautions to be taken in all cases in which a thermometer 
is used, in addition to those named, is to have a thermometer which 
is accurate, and to be sure that there is no acute or chronic inflam- 
matory process present which will produce local heat, and so give 
an erroneous impression as to the actual temperature of the entire 
body. This is particularly apt to be the case in diseases of the 
mouth in children: thus, stomatitis may raise the local temperature 



FE\ ER 445 

from 1° to 2°. Hot Liquids, if taken into the mouth just previous 
to or during the time at which the thermometer is inserted, will 
bo raise the temperature of the local tissues as to make the ther- 
mometer register several degrees above normal, and low records 
may be produced by cold liquids or ice held in the mouth. This 
subject has been studied by Lazarus-Barlow, who asserts that the 
effects of hot objects taken into the month last much longer than do 
those produced by cold, and that a mouth temperature should never 
be taken within one hour of the time that any hot food is ingested. 
lie even shows that holding the month open for some time renders 
a true estimate of the body heat impossible, and advises that the 
temperature shall never he taken in the month if it is possible to 
take it elsewhere. 

Febrile movements are generally associated with a dry, hot skin, 
hut sometimes with a cold, wet skin. 1 ne latter condition is of evil 
significance, as a rule, and should be remedied if possible. 

The Significance of Fever.— The significance of fever is 
great. It always shows the presence of an ailment sufficiently 
severe to make it wise for the physician to order the patient to 
bed until the fever abates or until he can surely determine it^ 
cause. The significance of a raised bodily temperature from a 
physiological point of view is that the nervous centres gov- 
erning heat production and heat dissipation arc 1 disturbed by some 
substance circulating in the blood or by reflex irritation, or perhaps 
by both. The danger of high fever is that it may cause morbid 

bo 

changes in the protoplasm of the heart or in the vital centres at the 
base of the brain, but the danger of ordinary febrile temperatures 
has been greatly exaggerated. Indeed, in some cases moderate fever 
probably aids the body in combating or, rather, conquering the dis- 
ease which has attacked it. This may occur in three ways, namely, 
by producing a temperature less favorable to the growth of certain 
disease germs than is the bodily temperature in health; by increasing 
cellular activity it may increase phagocytosis atid the development 
of antitoxic materials; and, finally, by virtue of the increased tem- 
perature, the effects of poisons may be rendered nil. This is the case, 
for example, in regard to the drug' digitalis, winch will rarely produce 
its ordinary effects on the heart when well-marked fever is present. 
Another point of importance in this connection is, that the dura- 
tion of fever has more to do with its importance as a symptom than 
has its degree, for a temperature of l()o° for a few hours may be 
borne with impunity, whereas one of 103° for many days cannot 
fail to produce evil effects. 

Fever in children does not possess nearlv as grave significance as 
it does in adults, for children often develop high temperatures from 
slight causes and have speedy recoveries. The balance of their heat- 



446 CHILLS, FEVER, AND SUBNORMAL TEMPERATURES 

mechanism is easily upset. The older the patient the greater the 
significance of fever, and a rise of 2° or 3° in a man of sixty years 
is more alarming than one of 4° or 5° in a child of five or six 
years. 

When fever is not due to a distinct pathological change in some 
part of the body, generally of an inflammatory kind, it may arise 
from a mild irritation of a mucous membrane, as when a catarrhal 
condition is set up. Such fevers are seen in cases of mild gastro- 
intestinal catarrh in children after the ingestion of bad food or expos- 
ure to cold. Sometimes fever apparently arises as the result of the 
reflex irritation produced by difficult teething (see chapter on the 
Mouth and Tongue) , although in many instances the fever of denti- 
tion depends upon a more or less closely related, but overlooked, 
gastric catarrh. Sometimes after a urethral sound or catheter has 
been passed into the urethra of a man, in the course of a few minutes 
or hours he develops a severe chill, followed by a fever which may be 
quite high, but which rarely lasts long. 

Fever in Infectious Diseases. 1 — Nearly all infectious diseases are 
ushered in by the development of fever of greater or less degree, 
and this is particularly true of the exanthemata. Inquiry should, 
therefore, be made by the physician as to the previous history of 
infectious disease. If one or more of the eruptive fevers have already 
been present, they can usually be excluded from the diagnosis of the 
illness present at the time of the visit. If, on the other hand, there 
is a history of pulmonary tuberculosis or acute articular rheu- 
matism, this may indicate that another attack is coming on. 

Typhoid Fever. — In typhoid fever the febrile movement is very 
characteristic in some cases, although in many instances it does not 
follow the description laid down in text-books. After several days 
of general wretchedness the patient develops a slight fever of from 
100° in the morning to 101° at night, and this temperature progres- 
sively rises so that the next morning it may be 101° and that night 
102°, the next morning 102°, that night 103°, and so on until the 
morning temperature may be 103° and the evening temperature 104° 
or rarely 105°. The fever usually reaches its acme by the end of the 
first week or ten days, and then for another week remains practically 
unchanged, there being a morning fall and evening rise of an almost 
equal extent. Toward the end of the third week, or sometimes 
earlier or later, according to the severity of the attack, the morning 
remissions become more marked, and then the evening rises fail to 
reach their former height. Often these marked morning remissions 
are the first indication of the tendency to recovery. Very high evening 
temperatures are indicative of a severe attack, but are not so indica- 

i Iu this connection the student should also read that part of the chapter on the Skin 
devoted to the consideration of the eruptive infectious diseases. 



FEVER 



447 



tive of serious illness as are high temperatures in the morning. After 
the third week, in a moderately severe case, the temperature falls 
gradually until by the twenty-eighth day it usually reaches the 

normal. In very rare cases the temperature speedily reaches its 
acme at the very beginning of the disease, and then passes through 
the course already described. Such eases are generally prolonged, 
hut may in some instances end by the fourteenth day. In other 
instances the development of high fever in the early stages of enteric 
fever, associated with severe general symptoms, is indicative of a 
short attack rather than a prolonged and severe one. 

Sudden falls of temperature during the course of typhoid fever 
are nearly always of grave import. The most common cause of such 
a sudden fall is an intestinal hemorrhage, and the fall may occur 
sometimes before the blood appears in the stools. In other cases 
such a fall is an evidence of intestinal perforation. The other causes 



8 — 

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Fig. 182. — Showing recrudescence of fever in a case of typhoid fever 

of a sudden fall are severe nose-bleed, or hemorrhage of any form; 
as, for example, that occurring in connection with abortion. Some- 
times, too, without any of these causes, the temperature falls very 
rapidly, and the patient goes into collapse. Such cases are very 
grave and the prognosis is unfavorable. 

A recrudescence or return of the fever, in which it rises quite rapidly 
to a point as high or higher than at any time during the attack, occurs 
in some persons who, during the stage of convalescence from typhoid 
fever, take solid food too soon, or are excited by the visit of a friend. 
Such rises are but temporary (Fig. 182). More rarely, as a result 
of getting out of bed too soon, or bad feeding, or other cause, a true 
relapse takes place, and the disease runs a second course, which is 
usually, but not always, of a shorter and milder character than the 
first attack (Fig. 183). Sometimes a mild, irritative fever, perhaps 
due to anemia, persists for some weeks, but the physician should not 



448 CHILLS, FEVER, AND SUBNORMAL TEMPERATURES 




31V0S JJ3HN3aHVd 



FEVER 449 

rest content with a belief that anemia is the cause until be has excluded 
all possibility of there being pulmonary, pleural, acute renal, or hone 
disease, as these conditions very commonly ensue as sequels of typhoid 

lever. In other instances, after the morning temperature has reached 
normal, the evening temperature remains pyretic for a number of 
davs, and this may persist for some time. In a number of instances 
I have known the use of strychnine in full doses, at this period of 
the disease, to produce ranges in temperature, which ceased as soon 
as the use of the drug was stopped. 

If the temperature in the course" of a case of typhoid fever rises 
as high as 107° or 108°, the prognosis at once becomes very grave. 

Very rarely enteric infection, so called, runs its entire course with- 
out any fever. Fisk, of Denver, and others have seen such cases, 
and the author had five of them at St. Agnes' Hospital in one term 
of service. 

Strumpell asserts that as a rare occurrence the fever in this disease 
may become intermittent, being normal in the morning and as high 
as 104° at night during almost the entire illness. 

The association of such a temperature curve as just described 
with the other characteristic signs of typhoid fever, as, for example, 
the development of the rose rash on the chest and abdomen, on or 
about the seventh day (chapter on the Skin ), the ochre-colored, loose 
stools, the peculiar stupid, drowsy appearance of the face, the 
Widal test, and in some cases the peculiar typhoid odor about the 
patient, all make the diagnosis certain. 

Irregular forms of malarial fever, particularly those forms due 
to infection by the estivo-autuinnal parasite 4 (see chapter on the 
Blood), may closely resemble typhoid fever. In many instances such 
cases are diagnosticated as typhoid fever, and probably some cases 
of true typhoid fever are thought to be malarial fever. The follow- 
ing differential table, drawn up by Thayer, is of interest in this con- 
nection. There is no such disease as typhomalarial fever, although 
there is no doubt, whatever, that pure typhoid infection may result 
in the production of a fever which closely follows the remittent and 
intermittent malarial types, and which is often associated with so 
much gastric disturbance and vomiting, and so lacking in the more 
prominent typhoid symptoms usually seen, that the picture of remit- 
tent malarial fever is clear, while the true picture of typhoid fever 
is clouded. 



Remittent Fever. 
Onset generally intermittent. 
Irregular remissions. 



Typhoid Fever. 
Onset gradual and progressive. 
Regular, though very slight morning remis- 
sions with evening exacerbations of tempera- 
ture. 
The temperature may arrive at 40° C. (104° The temperature does not reach 40° C (104° 
F.) within twenty-four hours. F.) before the third or fourth day, 

29 



450 CHILLS, FEVER, AND SUBNORMAL TEMPERATURES 



Remittent Fever. 

Headache rare in the beginning ; of a neu- 
ralgic character, pulsating, variable in its 
position and intensity. Sclera subicteric from 
the onset. 

The apathetic expression of the face, the dry- 
ness of the tongue, and sordes upon the teeth 
are not very marked. 

Breath foul. 

The delirium may come on in the early days ; 
it is recurrent, but changes with the exacerba- 
tions of temperature and other symptoms, and 
may give way to grave symptoms related to 
other organs. 

If there be pulmonary congestion, the cough 
and other symptoms come on suddenly ; the 
areas affected change from one to the other 
lobe or lung, and may disappear and reappear 
again with varying intensity ; dyspnoea is very 
pronounced ; circulatory disturbances are 
marked, even syncope. 

There are usually restlessness and anxiety 
(jactitatio corporis). 

Peculiar grayish color of skin ; sometimes a 
slight jaundice. 

Herpes common. 

Ansemia more or less marked early in the 
course. 



No characteristic exanthem 
uncommon. 



urticaria not 



At times there may be transient tympanites 
or ileo-csecal gurgling ; they are but slightly 
pronounced and paroxysmal ; diarrhoea is 
slight or absent, and has not the characters of 
that in typhoid fever. 

No distinct course. 

Urine high-colored; may show a trace of 
bile ; Ehrlich's diazo-reaction rarely present. 

Blood shows no leucocytosis ; eosinophiles 
not notably diminished ; serum does not cause 
agglomeration of typhoid bacilli (Pfeiffer, 
Durham, and Widal) ; malarial parasites and 
pigmented leucocytes present. 

Fever disappears under quinine. 

Is an endemic, disease occurring particularly 
in rural districts; rarely epidemic. 



Typhoid Fever. 
Headache from the beginning, permanent, 
severe, frontal. Sclera white. 



TUese symptoms are well marked and pro- 
gressive. 

Breath has a peculiar mouse-like odor. 

Delirium appears only when the disease is 
well pronounced ; it is often persistent, and 
variable only in degree. 



Pulmonary congestion is gradual and per- 
sistent ; always hypostatic (the bases and dor- 
sal surfaces of the lungs) ; the dyspnoea is less 
pronounced and later in appearing, depending 
more upon the abdominal conditions (tym- 
panites, etc.). 

There are usually relaxation, prostration, 
and stupor. 
No jaundice. 

Herpes rare. 

Ansemia absent, excepting in later stages. 

Characteristic roseola. 



Tympanites, gurgling, and diarrhoea appear 
slowly and may become well marked. 



Has a fairly characteristic course. 

Urine high-colored ; bile absent; diazo-re- 
action present during the height of the process. 

Blood shows no leucocytes ; eosinophiles 
diminished or absent; serum causes agglomer- 
ation of typhoid bacilli ; malarial parasites and 
pigment absent. 



Fever uninfluenced by quinine. 

Usually epidemic ; prevailing commonly in 
cities. 



Again, there can be no doubt that cases of true malarial infec- 
tion occur in which the symptoms so closely resemble those of 
typhoid fever that a purely clinical diagnosis is almost impossible, 
particularly if an epidemic of typhoid fever is in full swing at the 
time. Finally, there can also be no doubt that it is possible for the 
patient to have a double infection with the bacillus of Eberth and the 
Plasmodium of Laveran, in which case, however, the malarial mani- 



FEVER 451 

testations are usually dwarfed by the typhoid infection, and are only 
marked at the onset of the enteric fever and at its termination. To 
this mixed infection the term typhomalarial fever may be correctly 
applied to indicate not a separate disease, but a double infection. 
Etymologically, this term might also be used to define a condition 
of malarial fever in which, because of profound debility, the patient 
was in a typhoid state — that is, in a condition of which typhoid fever 
is a type. Practically, however, it should be discarded or limited in 
its use to the double infection just described. For Malarial Fever, 
see page 455. 

The febrile movement and other symptoms of enteric fever are 
often imitated very closely by those of ulcerative endocarditis. In 
addition to an irregular fever, there may be diarrhea, parotitis, 
stupor, and progressive feebleness in both diseases. An examination 
of the heart may reveal the presence of endocardial murmurs, which 
in association with signs of sepsis, or the existence of some focus 
of infection, such as a wound, a septic process, or the fact that the 
patient is in the puerperiuin, will render a diagnosis possible. (See 
also page 457.) 

Acute Tuberculosis. — The differential diagnosis of acute tuber- 
culosis from typhoid fever may be quite difficult in certain cases. 
When the symptoms of the two conditions are compared this is not 
difficult to believe, for we often have in both diseases headache, 
epistaxis, a very similar temperature chart, and a feeble pulse, while 
there may be in both conditions an eruption on the skin, which 
rather tends to confuse the physician than to aid him. Again, the 
delirium in each case is very similar, and the facial expression of the 
patient in both diseases is apathetic. Even the respiratory sounds 
in both diseases in their early stage may be apparently only those of 
a moderate bronchitis; and, finally, abdominal swelling, tympanites, 
and meteorism may occur in both maladies. Under these circum- 
stances the hereditary and recent history of the patient may be of 
much value, as showing a tendency to tuberculosis on the one hand, 
or exposure to typhoid infection on the other. Again, if it be typhoid 
fever, the spleen on percussion is nearly always found to be enlarged. 
Then, too, the lesions in the lungs of a typhoid fever patient are 
generally at the bases, while in tuberculosis they are oftener at the 
apices. The stools may be loose in both diseases, but in typhoid 
fever they are apt to be ochre-colored; and, again, in tuberculosis 
the loss of flesh is often exceedingly rapid, and profuse sweats and 
high fever are frequently seen. The mental apathy in typhoid fever 
is more marked, as a rule, than it is in tuberculosis. The finding of 
WidaFs reaction in the blood, or the discovery of the bacillus of 
Eberth in the feces and the presence of the diazo-reaction in the 
urine, would, of course, indicate typhoid fever. (See chapter on the 



452 CHILLS, FEVER, AND SUBNORMAL TEMPERATURES 

Urine.) An absence of leukocytosis would also indicate typhoid 
fever, for this condition is usually present in acute tuberculosis. 
Finally, careful and repeated examinations of the chest will usually, 
in the course of the disease, demonstrate the presence of tuberculosis 
of the lungs or bowels, if this be the cause of the illness. It seems 
hardly necessary to state that if any expectoration exists the sputum 
is to be carefully examined for tubercle bacilli in all doubtful cases, 
but while their presence proves tuberculous infection to be present, 
their absence does not prove the absence of this infection. 

Trichinosis. — An irregular fever with muscular pains and a great 
deal of discomfort in the belly, the case simulating typhoid fever, 
may occur in cases of trichinosis. 

Malta Fever. — A febrile movement closely resembling that of 
typhoid fever, a resemblance which is increased by the association 
with it of headache, insomnia, and anorexia, may be Malta fever, a 
disease which can be excluded in the vast majority of cases if there is 
no history of exposure to the exciting cause in the island of Malta, 
although it is not to be forgotten that Malta fever has been met with 
in persons returning from Porto Rico and elsewhere during the last 
few years. Sometimes it may be confused with relapsing fever, 
except for the longer febrile movement. Thus, after three or four 
weeks of illness convalescence seems to be established, and the tem- 
perature falls, but in a few days all the symptoms return with even 
greater vehemence than before. Such relapses may occur again and 
again. Violent pain in the joints on moving the body is often present. 
In doubtful cases the agglutination test with the blood may be per- 
formed, if it is possible to obtain cultures of the Bacillus melitensis. 

Typhus Fever. — The temperature chart of typhus fever is so dif- 
ferent from that of typhoid fever that it gives us a valuable differential 
point at the very beginning of the disease, for, after several days of 
languor, headache, and pain in the limbs, the fever suddenly springs 
on the patient, so that on the first night it may reach 105° F. Often 
it reaches 108° in a day or two, and while present is constant, the 
morning fall being very slight indeed. The development of the 
spots in a copious eruption on the third to the seventh day, which 
spots may develop into petechia? before fading, or remain unchanged 
in appearance, the great exhaustion, the severity of the illness, and 
the sudden rise of temperature, followed by a constant fever, point 
to typhus fever. Finally, the conclusion of the febrile movement, 
in favorable cases by the end of the second week, by crisis or by a 
more rapid fall of temperature than we are accustomed to see in 
typhoid, all help to make the differential diagnosis, which is, how- 
ever, in many cases very difficult or impossible in the early stages. 

Relapsing Fever. — The temperature of relapsing fever nearly 
always rises suddenly at the beginning of the attack to from 103° to 



FEVER 



153 



105°, and remains high with slight morning remissions from three to 
seven days, when it suddenly falls as by crisis to the normal or below 
it, after being on the preceding afternoon or evening unusually high. 
Sometimes it falls as low as 92° or 93°. The patient now remains 
free from fever for from several days to two weeks, when with a sud- 
den leap the fever and other symptoms of the first attack recur. A 
temperature of 105° to 100° in relapsing fever rarely indicates a 
grave outlook, as it does in typhoid. The only condition which 
resembles this temperature range of relapsing fever is intermittent 
malarial fever; but the rarity of relapsing fever in America, the 
frequency of malarial fever in certain parts, the presence of the 
spirillum of Obermeier in the blood in relapsing fever, and the 
malarial germ in the blood of intermittent fever, all make the 
diagnosis possible. 

Scarlet Fever. — In scarlet fever the temperature suddenly rises on 
the first day to 104° to 105°, and still higher on the next day, and 
then remains constant as long as the eruption is on the skin in full 



DAY OF 
DISEASE 


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Fig. 184. — Chart of scarlet fever. 



development. Just so soon as the eruption begins to fade the tem- 
perature also falls, not by crisis, but by lysis; not so slowly as in 
typhoid fever, but far more slowly than in croupous pneumonia 
(Fig. 184). This arrest of the fever usually takes place in simple 
cases by the end of seven days; and if it persists longer, is probably 
due to some complications, such as otitis, or the ''collar of brawn," 
due to enlarged cervical glands. The characteristic strawberry 
punctated rash and scarlet hue appearing on the first or second 
day, the ultimate dermal desquamation, the violence of the onset 
of the symptoms, the sore throat, and the peculiar appearance of the 
skin, all complete the clinical picture, particularly if the symptoms 
be in a child. (See chapter on the Skin.) 

In rare cases the fever in scarlatina is remarkably mild or almost 
absent, and these cases, as a rule, have a favorable prognosis. If 
the temperature be very high and persistent, on the other hand, the 
case is usually to be regarded as most grave. 



454 CHILLS, FEVER, AND SUBNORMAL TEMPERATURES 

Measles. — In measles the fever at first rises sharply to 103° or 
thereabout, then falls to a little above normal, is slight for several 
days, and then markedly increases with the development of the erup- 
tion on the fourth day, often ranging as high as 104° or 105°, at which 
point, with little variation, it remains for the two days during which 
the rash is well developed (Fig. 185). With the fading of the rash 
the temperature also falls by crisis. If fever persists to any extent, 
it is always due to some complicating cause other than the original 
disease; such a complication, for example, as a bronchial or gastro- 
duodenal catarrh. 




Fig. 185. — Showing initial fever with the subsequent fall and then a rise when the rash is well 
developed in a case of measles. Also shows an ending of the fever by crisis. 



Rotheln. — The fever of rotheln, if any occurs, is very seldom more 
than 102°, and has no typical preliminary rise as has measles, so 
that the temperature chart of the disease may aid materially in a 
differential diagnosis. (See chapter on the Skin.) 

Smallpox. — The febrile movement of smallpox is, with the excep- 
tion of that of typhoid, the most characteristic of all the eruptive 
diseases. With a sudden onset of fever, pain in the back, severe 
headache, and malaise, the patient takes to his bed if possible, and 
his temperature if taken will be found speedily to rise even to 105° or 
more in some cases, and then falls back to almost normal for two or 
three days, during which time the eruption appears. In this way, 
therefore, the temperature chart of variola differs diametrically from 
that of the eruptive fevers so far discussed, for in these cases the 
fever rises with the appearance of the eruption, whereas in this 
instance the temperature falls with the appearance of the eruption. 
This lower temperature persists for several days, from J° to 1° 
above normal, until the ninth day of the disease or the sixth of 



FEVER 455 

the eruption, when with the change of the pocks from vesicles to 
pustules the temperature rises again in what is called the fever of 
suppuration, which lasts with greater or less persistence for at least 
a week, when it ends by lysis or a gradual fall. Excessively high 
fever of 108° is a sign of approaching death or at least of very grave 
import. 

Varicella. — The febrile movement of varicella, or ehickenpox, is 
usually of very short duration and of little severity; but it may reach 
proportions entirely out of consonance with the general systemic 
disturbance, which is usually very slight in previously healthy 
children. Thus, it may rise in children who are prone to active 
febrile movements to as high a point as 105° for a very brief 
period, and yet may not seem to render the child ill. 

Erysipelas. — The temperature range seen in cases of erysipelas is 
quite typical. At the beginning of the attack the rise is quite prompt 
and sharp to 105° or 108° or even above this, and, instead of remain- 
ing constantly high through the course of the inflammatory process 
in the skin, goes through marked intermissions or remissions, which 
frequently occur and are followed by rises in temperature as high as 
that which occurred with the first onset. The fever ends in some 
cases by crisis and in others by lysis, the latter mode of ending 
usually taking place in those cases which have had a very severe 
attack prolonged in character, or which have been in an asthenic 
state prior to the disease. The diagnosis of erysipelas is easily 
made by the brawny, swollen, and red skin, with the peculiar line 
of demarcation at the edge of the swelling. (See chapter on the 
Skin.) 

Intermittent Malarial Fever. — A fever which rises sharply from 
normal to 103° or 104°, being preceded by a chill and followed in a 
very few hours by a sweat, the whole term of acute illness, if we 
exclude general physical discomfort, lasting but eight to twelve 
hours, is in the majority of cases that of intermittent malarial fever. 
The peculiarities of intermittent malarial fever, aside from those 
just named, are that the febrile movement begins to decline before 
the stage of sweating begins, and in some cases it begins to rise 
before the sensation of chilliness of the first stage leaves the patient. 
(See Fig. 18(3.) 

The fall of temperature is usually less abrupt than the rise, and is 
sometimes delayed by slight temporary rises or arrests in its down- 
ward course. The febrile movement is repeated at intervals, ranging 
from one to seven days or even at longer intervals than this. If the 
attacks occur daily, they are called quotidian, and this is due to 
infection by two sets of tertian parasites which undergo segmentation 
on alternate days, or it may be due to infection with three sets of 
quartan parasites. If the attacks occur every other day, they are 



456 CHILLS, FEVER, AND SUBNORMAL TEMPERATURES 

called tertian (Fig. 187); if on the third day, quartan; if on the 
fourth, quintan. If two attacks come on the same day, it is called 
double quotidian. 

Another point of importance in connection with malarial attacks 
is that they often occur earlier each day by an hour or more. Rarely, 
they are delayed. 

Intermittent malarial fever is to be separated from other inter- 
mitting fevers by a number of facts. First, the presence of the 
malarial organism in the blood at the time of the attack, or evidences 



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segmented at 8 p.m. and the second set at 4 p.m. Paroxysm stopped by quinine on fourth day. 



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Fig. 187.— Showing paroxysms of tertian fever, the segmentation of the organism occurring at 
about twelve o'clock every other day. 

of its presence at other times. (See chapter on the Blood.) Second, 
by the history of exposure to malarial influences. Third, by the 
marked effect for good on malarial fever produced by the adminis- 
tration of quinine. 

As stated in the chapter on the Blood, an examination of this 
fluid will reveal in practically every form of infection, except malaria 
and typhoid fever, an increased leukocytosis; but in malarial infec- 
tion the leukocytes are not increased in number. 

Care must always be taken that the intermitting fever of the 



FEVER 457 

various forms of sepsis is not diagnosticated as malarial intermittent 
fever. The most common error of this character is the making of 
a diagnosis of irregular malarial intermittent, because chills, fever, 
and sweat appear every evening, when, in reality, the real cause is an 
undiscovered pulmonary or abdominal tuberculosis. Again, acute 
ulcerative endocarditis and purulent phlebitis may cause similar 
symptoms, as may also hepatic abscess, impaction of gallstone-. 
with suppurative cholangitis, causing the so-called Charcot's fever 
below). The absence of a history of malarial exposure, the 
possible presence of a cough, and the discovery of a tuberculous 
Lesion in the chest or abdomen by careful physical examination will 
aid in deciding that the fever is tuberculous and not malarial in origin. 
(See chapters on the Thorax and on the Abdomen.) 

Ulcerative Endocarditis. — The temperature curve may exactly 
resemble intermittent malarial fever; but in many instances the 
presence of an external wound, acute sepsis in some part of the 
body, or the presence of the puerperium will reveal the source of 
an infection. (See Fig. 188.) In the typhoid type of ulcerative endo- 
carditis the profound asthenia and general prostration will separate 
the disease even if the temperature chart be useless. In this form 
the febrile movement is rarely typically intermittent. The crucial 
test of the differential diagnosis lies in an examination of the heart, 
in which a murmur may be heard in some but not in all cases, unless 
there has already been some grave valvular mischief. The cardiac 
feebleness and asthenia, on the one hand, and the result of the blood 
examination, on the other, aid the diagnosis. The duration of the 
case is not of much value in making a diagnosis, for cases of ulcera- 
tive endocarditis have lasted from two days to more than a year. 
Rarely, it lasts more than six weeks. Death usually occurs in ulcera- 
tive endocarditis, unless there has been previously present chronic 
endocarditis, in which case recovery may rarely occur. 

The discovery of some spot showing a phlebitis may point to this 
cause for intermittent fever. 

The fever of catarrhal or suppurative cholangitis often closely 
resembles intermittent fever, but the presence of hepatic symptoms, 
of marked jaundice, of a history of gallstone colic, and of exceedingly 
severe rigors, enables us to separate them. In obscure cases the 
malarial organism should be searched for, and if the condition be one 
of cholangitis an examination of the blood will probably show leuko- 
cytosis. (See chapter on Pain, Gallstone Colic.) 

When fever of an intermittent type has been observed, and inter- 
mittent malarial fever, tuberculosis, and cholangitis cannot be dis- 
covered as a cause, search should be made for tenderness and swell- 
ing of the liver due to hepatic abscess. Profuse sweats also may be 
found in such cases, as in most instances of septic fever. The diag- 



458 CHILLS, FEVER, AND SUBNORMAL TEMPERATURES 







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PLATE XVI. 





Hodgkin's Disease. (De Forest's Case.) 



FEVER 159 

Qosis of hepatic abscess will be strengthened if there is a history of 
the patient having suffered from dysentery, as hepatic abscess is 
sometimes caused by amebic dysentery. 

The presence of fever preceded by chills, the temperature rising 
to 104° or even 105°, followed by excessive sweats, in a person who 
is profoundly cachectic, may be due to pernicious anemia or to septic 
poisoning, as already pointed out; and it should be recollected that 
such a temperature chart is sometimes seen in cases of gastric cancer. 
Similar symptoms as to fever in association with enlargement of the 
lymphatic glands, particularly those of the neck, indicate Hodgkin's 
disease (see chapter on the Blood), or even more commonly tuber- 
culous adenitis, which, however, is usually met with in the young 
and involves the glands near the jaw, while in Hodgkin's disease the 
glands near the clavicle are affected. Further, in Hodgkin's disease 
the swelling is usually bilateral, and to be found elsewhere than in the 
neck. (See Plate XVI.) Again, in tuberculous disease these glands 
often suppurate. The presence of the tubercle bacillus in an excised 
piece of the swelling will decide the diagnosis. In the opinion of 
some clinicians the two states are identical in cause. An intermittent 
fever may also be seen in suppurative pyelitis, in association with 
pyuria. This pyelitis may or may not be tuberculous. 

Remittent Malarial Fever. — Remittent fever rising and falling 
every few days for two or three weeks, rarely rising above 103° to 
104°, and even falling to the normal line, associated with enlargement 
of the spleen and liver, yellowing of the skin, or jaundice, bilious 
vomiting, and a history of exposure to malarial infection, is char- 
acteristic of remittent malarial fever, a form more chronic and very 
much more grave than the intermittent form just described, because 
it responds less readily to treatment; and, secondly, because it is 
accompanied by more marked changes in the viscera. It depends 
upon infection with the estivo-autumnal form of the malarial parasite. 
The conditions produced by this parasite are collectively grouped 
under the names remittent, continued, bilious remittent, and typho- 
malarial fever, or malarial fever of a typhoid type. In some cases 
the temperature and other symptoms will so closely resemble those 
of typhoid fever that nothing short of an examination of the blood 
can decide the diagnosis. (See chapter on the Blood.) 

Care should be taken to recollect the fact that when typhoid fever 
develops in a young child the temperature may be so markedly 
remittent that an erroneous diagnosis of malarial infection may be 
made. In other words, "infantile remittent fever" is really typhoid 
fever in many instances. 

A febrile process somewhat closely resembling remittent malarial 
fever, yet so rare, comparatively, as never to be confused with it, is 
Weil's disease. In this condition the fever runs a remitting course, 



460 CHILLS. FEVER, AND SUBNORMAL TEMPERATURES 

is associated with jaundice and swelling of the liver and spleen, and 
the stools may be clay-colored. There is one important point of 
difference between malarial remittent fever and Weil's disease, 
namely, that in the latter gastro-intestinal symptoms are nearly 
always wanting or are mild, whereas in the former they are apt to 
be marked. Usually the fever of Weil's disease ceases by the end of 
two weeks or earlier. It is probably an infectious jaundice-. 

Dengue. — In dengue, a disease seen most commonly in epidemics in 
certain parts of the southern United States, the patient, after suffering 
from violent aching pains in the body and limbs, swelling of the joints, 
and the development of a variable rash on the chest, develops an 
active fever, which lasts with the pain until the fifth day, when both 
the pain and fever decrease or cease, and then often return with equal 
force. These facts, combined with the fact that it is an epidemic 
disease, separate it from malarial fever. Dengue and influenza, of 
an epidemic type, closely resemble one another, but in dengue 
there is rarely marked involvement of the respiratory tract as there 
is in influenza; there is an eruption which is not seen in influenza, 
and it is not followed or accentuated by such grave complications as 
we see in the more severe cases of influenza. Dengue is a disease of 
the South and influenza one of the North. 

Yellow Fever. — The fever of yellow fever is rarely over 103° or 
104°, and is one of the milder symptoms of the disease; but it pos- 
sesses this peculiarity, namely, that after the lapse of from twelve 
hours to several days there is a marked remission of the fever and 
all the other symptoms, and from this time on the patient may get 
well, or after a few hours this calm stage is followed by the true 
violent symptoms of the disease, such as black vomit, tarry stools, 
jaundice, and hemorrhages from the mucous membranes. Gener- 
ally the full course of the disease to convalescence or death is run in 
about one week. 

There are only two other diseases which can be readily confused 
with yellow fever, namely, dengue and bilious remittent fever. 
Dengue has been confused with yellow fever many times, and even 
the most experienced physicians have had great difficulty in sepa- 
rating them when the yellow fever has been mild. The most impor- 
tant points in their differentiation are the facts that in dengue there 
is usually a second onset of fever several days after the first onset, 
whereas this does not occur in yellow fever. Again, the eruption on 
the skin is not seen in yellow fever, and a rapid pulse is present in 
dengue, whereas in yellow fever the pulse is usually not very rapid. 
On the other hand, in yellow fever we usually meet with jaundice, 
albuminuria or suppressed urine, and a hemorrhagic tendency of a 
marked degree, all of which are absent in dengue. Further, death 
from dengue is very rare. 



FHVUli 



461 



A case' o 
yellow 



)lllOUS 



emittent fever occurring (luring an epidemic of 

fever is almost certain to be incorrectly diagnosticated. In the 
absence of an epidemic, however, the probabilities of the case being 
bilious remittent fever are very great, and the presence of bilious 
vomiting rather than that of blood, the characteristic temperature 
chart, and, above all, the presence of a history of malarial exposure 
and of the signs of malarial infection in the blood, with the partial con- 
trol of the symptoms by quinine in certain stages of remittent fever, 
point to the diagnosis of malarial disease rather than to yellow fever. 
Stubbert gives the following differential tables of these fevers: 



Yellow Fever. 

Headache bilateral-frontal, and post-orbi- 
tal. 

Temperature and pulse divergent; temper- 
ature rarely higher than 104° F. 

Albumin present in large quantities early 
in the disease. 

Quinine has no effect on the progress of the 
disease. 

Stage of remission on third or fourth day. 

Attacks new arrivals. 

Always history of exposure to infection. 
Black vomit appears on third or fourth day. 
Hematuria very rarely present. 
Liver unchanged. 

Yellow Fever. 

Cephalalgia and nephralgia are character- 
istic and constant. 

Pulse and temperature divergent. 

The slowing of the pulse begins early in the 
disease. 

Congestion of face early in the disease. No 
edema. 

Albuminuria. 

Icterus. 

Black vomit. 

No eruption. 



Pernicious Malaria. 

Headache generally unilateral-frontal, and 
temporal. 

Temperature and pulse correlative; tem- 
perature generally 105' to 107° F. 

Albumin rarely present. 

Quinine has a specific effect if given hypo- 
dermically and early. 

Remission not present. 

Generally history of Chronic malarial in- 
fection. 

No history of exposure to infection. 

Black vomit appearswithin thirty-six hours. 

Hematuria a marked Bymptom. 

Liver enlarged and tender. 

Dengut Fever. 

Pain most severe in joints and muscles, and 
is paroxysmal. 

Pulse and temperature correlative.' 

The slowing of the pulse occurs late in the 
disease. 

Rash on face, followed quickly by edema. 



Albuminuria absent. 
Icterus absent. 
Black vomit absent. 
Polymorphous eruption, 
quamation. 



followed by des- 



Cerebrospinal Meningitis. — Just as in yellow fever, so in spotted 
fever or cerebrospinal meningitis of an epidemic form, the fever itself 
is one of the least important symptoms, for, aside from the fact that 
it is apt to be irregular and intermitting, it is rarely very high, as 
compared with the violent cerebrospinal symptoms, the rigidity of 
the back of the neck, the headache, convulsions, and vomiting. The 
presence of these symptoms in an epidemic does more to confirm a 
diagnosis than the febrile movement. In some cases of spotted 
fever, however, of a very grave type, the fever becomes a hyper- 
pyrexia, but in cases tending toward recovery the temperature usually 
begins to fall by lysis before any moderation in the other symptoms 
is manifested. 



462 CHILLS, FEVER, AND SUBNORMAL TEMPERATURES 

When the physician feels it necessary to determine the true char- 
acter of the affection without delay, he may resort to lumbar punc- 
ture. An ordinary aspirating needle is introduced between the second 
and third, or third and fourth lumbar vertebrae (Fig. 27), and by 
this means some of the cerebrospinal fluid is obtained, which should 
be received in a sterile test tube, and examined microscopically for 
the characteristic diplococci of spotted fever, and for other micro- 
organisms. The needle should be inserted 4 cm. (lj inches) in 
children, and 6 to 8 cm. (2 to 4 inches) in adults, to reach the fluid 
around the cord. It is not a dangerous operation. Pfaundler, on 
the other hand, recommends that the puncture be made in the 
lumbosacral space, and that it should be performed while the 
patient is in the sitting position. (For area for puncture see the 
figures on the spinal column in the chapter on the Feet and Legs.) 

He believes that very high pressure of the fluid in the spinal mem- 
branes is present in tuberculous meningitis, and that this high 
pressure is so rare in other conditions that its presence is of diagnos- 
tic value. It is found, however, when the patient is suffering from 
purulent meningitis, from spinal tumor, and in some cases of func- 
tional neurosis. On the other hand, normal pressure excludes the 
presence of meningeal or cerebral affections. If the fluid which is 
obtained contains disintegrated blood, the patient is probably suf- 
fering from pachymeningitis or injury. If, on the other hand, the 
blood is fresh in its appearance, its presence is probably due to the 
puncture. 

A very important point in this connection, insisted upon by 
Pfaundler; is that if the fluid is clear, every inflammatory affection 
of the meninges, except tuberculosis, may be excluded from the diag- 
nosis. In tuberculosis, it is often cloudy, and in the later stages of 
the disease nearly always so. If the fluid is purulent, it indicates 
the presence of purulent or epidemic meningitis. A clear fluid is 
found in health, in serous meningitis, hydrocephalus, and functional 
neuroses, and it is generally clear in cases of tumor, uremia, and 
sepsis. The albumin present varies from 0.02 to 0.04 per cent., and 
if it is in excess of 0.05, it is probable that the disease is an inflam- 
mation or tumor; if it is present in still larger amounts, it is probably 
tuberculous meningitis. If, again, on analysis of the fluid the normal 
sugar which it contains should disappear, there is probably an inflam- 
matory process present, and therefore if sugar is present an inflam- 
mation can be to a certain extent excluded. 

Even in the presence of an epidemic of spotted fever it should 
never be forgotten that middle-ear disease often causes marked 
meningeal symptoms, and that croupous pneumonia often produces 
a similar train of manifestations, probably by infection with its 
particular microorganism. The possibility of tuberculous infection 



FEVER 



463 



producing such symptoms should cause the physician to examine the 
patient carefully for signs of tuberculous disease in other parts of the 
body from which infection might arise, as, for example, the lungs. 
Septicemia. — The fever due to septicemia may produce a tempera- 
ture chart which closely resembles that of enteric fever, but septic fever 
generally possesses one characteristic which, in the face of other symp- 
toms suggesting sepsis, is of great importance, namely, the extraordi- 
nary rises from normal to 105° or 108°, and from that point even to a 
subnormal degree within a very few hours, so that the lines on the 
chart pass up and down in long sweeps. These sweeps are even more 
sharp and sudden than in an intermittent malarial fever, and their 
cause is determined by the discovery of some septic process in some 
part of the body. The presence of such a chart, in association with 
dull or violent headache, delirium, vertigo, and vomiting independent 
of taking food, would point to cerebral abscess, particularly if a 
history of injury could be obtained. 




Fig. 189. 



-Chart of a case of pulmonary tuberculosis, showing rising and falling of the 
temperature morning and night. 



A somewhat similar chart to this may occur in connection with 
cases of active pulmonary tuberculosis, when the lesions are well 
developed and septic absorption is active; but usually in the hectic 
fever of phthisis we have an approximately normal morning tem- 
perature, with a rise from 2° to 3°, or even more, toward night 
(Fig. 189). 

This symptom of fever in any form occurring in a person with 
suspiciously "weak lungs" should cause the physician to be confi- 
dent that he has overlooked some focus which another careful exam- 
ination may discover, and it possesses another important diagnostic 
significance, namely, that the more active the febrile movement in 
phthisis pulmonalis the more active the disease process, and the less 
active the fever the less active the process. Fever may, however, 
be almost entirely absent in some tuberculous cases with extensive 
disease of the lungs. 



464 CHILLS, FEVER, AND SUBNORMAL TEMPERATURES 



Acute Miliary Tuberculosis. —The febrile movement of acute miliary 
tuberculosis has nothing characteristic about it, except that in some 
cases it may closely resemble that of typhoid fever, and if the physician 
does not carefully examine the case an erroneous diagnosis may be 
reached. If, however, the disease involves the meninges of the brain, 
a hyperpyrexia may be developed, and death speedily occurs in such 
cases, either in the fever or in a sudden collapse. The peculiar 
dyspnea, the cyanosis, the profuse sweats, and the diffuse pulmonary 
signs render a diagnosis of acute miliary tuberculosis possible in some 
cases. 

Influenza. — When fever is associated with marked catarrhal symp- 
toms, chiefly of the bronchial tubes and upper respiratory tract, 
with sneezing, lassitude, pains in the back and limbs, and exces- 
sive cough, the fever rising as high as 104° or 105° in severe cases, 
and then falling almost to normal, we may have before us influenza 
or catarrhal fever either of the sporadic or epidemic form. In this 
condition there may be in severe cases great prostration and 
cardiac failure or vomiting and diarrhea. The febrile movement 
is of the most irregular type, even when some grave complica- 
tion, such as severe bronchitis or pneumonia, comes on, although 
croupous pneumonia rarely occurs as a complication of "la 
grippe." 

Hay Fever. — The respiratory symptoms just described are also seen 
frequently in association with moderate fever, in " hay fever," that 

condition seen in susceptible persons 
during the haying season or late in the 
summer. 

Croupous Pneumonia. — The fever of 
acute pneumonia of the croupous type 
runs a very typical course in uncom- 
plicated cases. Following a more or 
less severe chill, the fever quickly 
mounts to the high point of 103° or 
104°, or even more than this (Fig. 190). 

Fi^So^ch^ftS^fS^ous For tne ne . xt few davs > if not modified 
pneumonia, showing primary rise of by the antipyretics and the use of cold, 
temperature to 103 4 o and crisis occur- the fever remains high; but there mav 

ring as early as the third day. . . °. ," 

be temporary remissions which look 
as if crisis was about to be established, when in reality they 
are followed at once by a return of the fever (pseudocrisis). 
Finally, in the majority of cases of croupous pneumonia the tempera- 
ture suddenly falls by crisis on the seventh to ninth day (Fig. 191), 
and convalescence is established, although the sudden fall of fever 
may be associated with dangerous collapse. Sometimes convales- 
cence is broken by brief and slight febrile movements. If the case 




/•/•; i ER 



165 



has been prolonged, or if it is of the typhoid type, the fever may end 
by lysis. 

Catarrhal Pneumonia. — It is to be remembered that the fever of 
catarrhal pneumonia is rarely as high as in the croupous form, 
usually 101° to 103°, and ends by lysis, not crisis. Sec chapter on 
the Thorax.) 

The fever of acute bronchitis possesses no peculiarities over that 
of other acute inflammations. 



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Fig. 191. — Chart of a ctise of croupous pneumonia, with crisis on the seventh day; admitted 
to the author's ward on second day of illness. 

Syphilis. — It is not proper to leave the subject of fever due to the 
various infectious diseases without calling attention to that due to 
syphilis in the secondary period of its course. With the onset of the 
roseola or other skin lesion a fever, more or less marked, is nearly 
always present and is often preceded by chilly sensations and general 
malaise. This febrile movement may then follow one of three 
courses: it may never rise above 101°, and proceed as does a simple 
fever, with slight morning remissions and evening exacerbations; or 
it may be as remittent as is a malarial remittent fever; or, again, it 
may resemble a malarial intermittent, rising to a high point and 
then falling almost to the normal. Phillips, of London, has reported 
a case of syphilitic fever in which this febrile movement lasted for 
weeks, and, after being treated by quinine as a supposed tertian 
ague, ended at once under antisyphilitic medication. (See chapter 
on the Skin, Eruptions.) 

Acute Articular Rheumatism. — The fever of ordinary cases of acute 
articular rheumatism is usually moderate, rarely exceeds 103°, 
and possesses no typical characteristics; but in very severe forms 
30 



466 CHILLS, FEVER, AND SUBNORMAL TEMPERATURES 

of the disease with cerebral manifestations, a rheumatic hyperpyrexia 
may be developed, when, with delirium, convulsions, and cyanosis, 
the fever rises to 106° and even to 108°, after which death often 
ensues. The history of previous attacks of articular rheumatism, 
the hot, swollen joint or joints (usually the large ones), and the suc- 
cessive invasion of other joints as the ones first affected .get well, 
point to the correct diagnosis. It must not be forgotten, however, 
that gonorrheal and other forms of septic arthritis occur with febrile 
movement. Pyemia, osteomyelitis, and purpura also may produce a 
fever with swelling of the joints. (See chapter on the Legs and Feet.) 

Thermic Fever. — When a person, previously afebrile, during hot 
weather or when exposed to artificial heat in excess, is attacked by 
unconsciousness, convulsions, and very high fever, he is probably 
suffering from thermic fever or heat-stroke. Theoretically similar 
symptoms might be caused by a lesion due to embolism or hemor- 
rhage in the neighborhood of the pons Varolii, but this is very rare. 
(See chapters on Hemiplegia and the Face and Head.) The fever in 
sunstroke may rise as high as 110° or 112° or even more; the skin is 
hot and dry, or more rarely cold and moist with sweat; but, even if 
this is the case, the rectal temperature will be found hyperpyretic. 

A great rise of temperature (110° to 112°) often occurs after 
injuries to the cervical region of the spinal cord. 

Acute Multiple Neuritis. — The rapid development of fever, pain in 
the back and limbs, and particularly in the nerve trunks, the tem- 
perature soon reaching 103° or 104°, may be due to an attack 
of acute multiple neuritis, and the history that the illness has 
followed exposure to cold and wet may, on the one hand, make 
the physician believe that his case is suffering from rheumatism 
or influenza, or on the other, in the absence of such a history, 
from the early stages of one of the infectious diseases. The early 
appearance of tingling, numbness, loss of power, and wasting of 
the muscles soon decides the diagnosis in favor of neuritis. The 
nervous disease which most closely resembles acute febrile neu- 
ritis is Landry's paralysis, and a differential diagnosis may be 
difficult; but in neuritis there are loss of sensation, muscular wasting, 
signs of degeneration, and fever, whereas in Landry's paralysis all 
these are wanting, excepting the sensory symptoms, which in both 
diseases may be similar. The predominant symptoms of Landry's 
paralysis are paralysis and loss of reflexes. (See chapter on the Legs 
and Feet.) 

The prognosis of the severe form of febrile neuritis is grave, as 
death may ensue from respiratory paralysis. 



SUBNORMAL TEMPERATl RE 467 



SUBNORMAL TEMPERATURE. 

Subnormal temperature of the body is seen as the result of 
any profound nervous shock, as after an accident or surgical opera- 
tion, or prolonged anesthetization. It occurs, too, at the ending 
of the fever of croupdus pneumonia and other febrile movements 
ending by crisis. It is also seen in severe cholera morbus and 
cholera Asiatics and sometimes in cholera infantum, and often 
is present either in the early part of the cold stage of intermittent 
malarial attacks or more commonly after the fever of the attack has 
fallen. A subnormal temperature of a dangerous degree is met 
with in the algid type of pernicious malarial infection, and can only 
be satisfactorily differentiated from other conditions by a blood 
examination. Subnormal temperatures are also seen in some cases 
of confusional insanity and of tuberculous meningitis and hysteria. 

Heat Exhaustion. — An important variety of subnormal tempera- 
ture is that seen in the form of heat-stroke called heat exhaustion, 
when, in place of fever, a condition of collapse is induced. 

Severe injury to the dorsal region of the spinal cord often produces 
a great fall of temperature. 

A temperature below 92..']° is nearly always fatal in its prog- 
nosis, but subnormal temperatures above this degree are not neces- 
sarily followed by death. A temperature of 95° IS spoken of as 
one of moderate collapse. 



CHAPTEE XV. 

HEADACHE AND VERTIGO. 

The causes of headache — Digestive headache — Headaches due to the eyes — 
Headaches due to cerebral growths and abscess — Headaches due to syph- 
ilis — Headaches complicating acute diseases. 

HEADACHE. 

Headache is, of course, always a symptom and never a disease, 
and it arises from such widely different causes that it is impossible 
in this book to discuss all of them. Only the more common condi- 
tions resulting in its development can be considered, more particu- 
larly in relation to its diagnostic significance in serious pathological 
states. The most common cause of headache is probably disorder 
in the function of the digestive apparatus, the next most common 
cause is eye-strain in its various forms, and the third is nervous 
exhaustion or neurasthenia with or without associated anemia. 
These may all be considered as perversions of function causing 
headache — that is, the pain in the head may be termed a functional 
headache. Less frequent, but far more important from a diagnostic 
standpoint, is headache seen in persons suffering from renal disease, 
brain tumor, and meningitis in its various forms. The remaining 
causes of headache are numerous, and some of them will be con- 
sidered later; but the most important of the first class are the head- 
aches of the gouty or the rheumatic, and of the second class those of 
cranial periostitis, middle-ear disease, and acute inflammation of 
the eye or in the jaw. 

Headaches depending upon disturbance of the digestive system are 
nearly always accompanied by evidences of such disorder, consisting 
in gastric or intestinal distress, belching, hiccoughing or vomiting, 
or even by diarrhea. Often there is a distinct history of the ingestion 
of indigestible food or digestion-disturbing drink, but in other cases 
exposure to cold so congests the abdominal viscera that catarrh of the 
stomach and bowels is induced, and with it congestion of the liver 
followed by jaundice. The headache of disturbed digestion is 
nearly always frontal, and in many cases congestive to such an extent 
that the face may be flushed, or at least the intracranial circulation 
is so disturbed that the patient is unable to lower the head, because 
such a posture increases the pain. Such cases are relieved by hot 



HEADACHE 469 

foot baths which relieve the congestion of the head; nearly always 
by the act of vomiting, which should he induced, if need be, by an 
emetic or by putting the finger into the back of the throat. Vomiting 
makes such headaches very much worse for a time, owing to the con- 
gestion of the head following the efforts at vomiting, and this is an 
important point in diagnosis, for in uremia due to renal disease and 
in some other states the vomiting is often so easily performed that 
no straining accompanies it. 

That disturbances of the digestive tube are capable of altering 
the intracranial circulation is proved by numerous facts. Thus 
Brunton quotes the experiments of Ludwig and Dogiel, who showed 
that moving the intestines by the finger introduced through an 
abdominal incision caused a great increase in the flow of blood 
through the carotid arteries. 

Headache due to disorder of the digestion rarely ensues immedi- 
ately after food is taken, since some time must elapse before the 
ingested material becomes changed into an irritating or toxic mass 
by fermentation or putrefactive processes. As a consequence, several 
hours or even a day may pass without any discomfort in the head, 
after which time the full force of the headache develops. The head- 
aches of indigestion are, however, characterized by two important 
facts, viz., that they are not constant, and, second, that they are 
often relieved or prevented by the use of a purgative, even if consti- 
pation has not been present. Such headaches are very apt to be 
pulsating and accompanied by great nausea. Sometimes such a 
headache takes a form called migraine or hemicrania, a condition in 
which the pain is chiefly, if not entirely, unilateral, and there is 
associated with the pain early and more or less persistent hemi- 
anopsia. It is to be remembered, however, that in some cases of 
hemicrania of nervous origin the sickness at the stomach seems 
to be secondary to the severe pain in the head. 

Headaches resulting from digestive disturbance do not always 
depend entirely upon irritation of the stomach and bowel with reflex 
disturbance of the circulation and sensory nerves of the head, but 
upon the absorption of poisonous substances formed in the digestive 
tube. These poisons are usually formed only to be destroyed by 
the liver, or are developed in too small quantities to have any effect ; 
but no sooner do congestion of the liver and deficient biliary secre- 
tion ensue than they are formed in large amounts, and enter the 
general blood stream, owing to the absence of antiseptic bile and 
the coincident or consequent constipation. As a result, we see very 
violent headache in jaundice due to catarrhal changes, particularly 
if the kidneys are not active in the elimination of toxic substances. 
Similar symptoms to those just described may occur in cases suffer- 
ing from paroxysmal hemoglobinuria, for in this state severe head- 



470 HEADACHE AND VERTIGO 

ache, nausea, vomiting, and persistent yawning are often present, 
with an icteroid discoloration of the skin. The reddish urine, pain 
in the liver, and sometimes an urticarial eruption will aid the diag- 
nosis of this primary hemoglobinuria. 

In other cases in which no jaundice is present violent headaches, 
which utterly incapacitate the patient, come on from auto-intoxica- 
tion. Thus, a man apparently perfectly well goes to bed on a certain 
night and wakes in the morning feeling a little more drowsy than 
usual. On rising he may feel a little stupid, and perhaps be slightly 
vertiginous, but is able to eat his breakfast as heartily as usual. In 
the course of a few hours the mental heaviness becomes more marked 
and a pain in the brow develops, which gradually gets worse and 
worse until it is unbearable. The ordinary remedies for neuralgic 
headache are futile, and he finds no relief until by the use of a purga- 
tive he removes the source of his intoxication, and his kidneys have 
time to eliminate the toxins already absorbed. Sometimes vomiting 
comes to his relief, and the emptying of the stomach so stimulates 
his liver and intestines by the efforts of vomiting that the process of 
auto-intoxication ceases. Some of the intestinal poisons have been 
isolated by Brieger, Harnack, and others, and have a physiological 
action like many well-known drugs. Thus, one produces effects like 
those of digitalis, another like those of belladonna, and a third like 
those of aconite. Pulsating pain and a slow, full pulse may indicate 
the absorption of the digitalis-like toxin; a flushed face and hot, 
dry skin, the belladonna-like toxin; and pallor, faintness, and a 
feeble pulse, if no nausea is present, the presence of the aconite-like 
toxin. Persons suffering from headache of this type are nearly 
always much freer from discomfort in the head after such an attack 
than they have been for some time before. 

Brunton has also pointed out that digestive headaches are often 
associated with an objective and subjective sensation of increased 
intra-ocular tension and tenderness on the upper surface of the eye- 
ball, and the author has frequently confirmed this observation. 

The headache of eye-strain is usually due to abnormalities in the 
ocular muscles. Most commonly, according to Noyes, the externi 
(abductors) are the muscles which are the seat of the difficulty, but 
this opinion is not generally shared by other ophthalmologists, who 
assert that the interni are most commonly at fault. Such headaches 
may be felt in any part of the head, but are most commonly said to 
be in the occipital region. If, in association with such headache, 
immediately after or long after reading there is blurred vision, pain 
in the muscles of the eye on suddenly moving the eyeball, a ten- 
dency to congestion of the lids, or hyperemia in the conjunctiva over 
the insertion of the muscle, the diagnosis of headache from eye-strain 
is practically certain. (See chapter on the Eye.) Violent pain in the 



HEADACHE 471 

head may also be due to irritable retina and to astigmatism and 
spasm of the eiliary muscle. Acute inflammatory processes in any 
part of the eye may produce severe headache, particularly iritis, the 
pain of which is very apt to be worse at night. 

Violent headache is often produced by acute or chronic glaucoma, 
and is usually felt about the eyes or orbit. Often it is of a unilateral 
character, and the sharp, shooting pain causes a false diagnosis of 
neuralgia to be made, or in some cases the patient is thought to be 
suffering from migraine, because in addition to unilateral pain there 
are often nausea, vomiting, and pallor of the face. The examina- 
tion of the eye will show glaucoma to be present. Quite similar 
symptoms may appear as the result of a foreign body lodged in the 
cornea. 

The headache associated with nervous exhaust ion or neurasthenia 
may be superficial or deep; that is to say, neuralgic or apparently 
within the skull. It is often associated with some dizziness and ver- 
tigo, and is nearly always occipital in character, more rarely appear- 
ing over the brows. In addition to the pain, which is generally not 
very severe, there is often a sense of constriction about the head. 
Such a headache persists as long as a person who is overworked 
persists in fatiguing himself, and rapidly disappears when rest is 
taken. More rarely the pain in the head in neurasthenia is that of 
migraine, and is complicated by hemianopsia and hemicrania, often 
by a dilated pupil on the affected side, and flushing and pallor of 
one side of the face. 

Headaches due to rheumatism are often quite severe, and are asso- 
ciated with much tenderness of the scalp or muscles covering the 
skull. Similar headaches, but more dull in character, are also seen 
in persons suffering from phosphaturia, and are relieved by benzoate 
of ammonium. 

A headache is a symptom very commonly seen in persons who are 
subject to the chloral habit, and it may be general or limited to the 
forehead. It is commonly associated with vertigo, flushing of the 
face, and intense heaviness and drowsiness. 

Headache of a violent, bursting character may be produced by 
full doses of nitroglycerin, the salicylates, and quinine, and by the 
use of large quantities of tobacco. 

Leaving the headaches due to functional disturbances not associ- 
ated with organic change, we pass to those due to organic disease. 
Those due to renal disease are of two classes, in that they are an evi- 
dence of uremia, or they are congestive and due to the high arterial 
tension so often seen as the result of chronic contracted kidney with 
its associated conditions of cardiac hypertrophy and arteriosclerosis. 
Uremic headache, as pointed out in the chapter on Vomiting, is 
often associated with nausea or vomiting of a persistent type, and 



472 HEADACHE AND VERTIGO 

sometimes with diarrhea, for purging is an effort at elimination. 
The pain is not of the shooting, darting, or neuralgic type, but dull, 
even if severe, and is often associated with a sensation of fulness in 
the head. Sometimes the tendency to drowsiness is very marked, 
and, even if the patient does not sleep, he may seem on the verge of 
sleep all the time. Not rarely these cases instead of becoming coma- 
tose become wildly delirious. 

These uremic headaches may occur in any form of renal disease, 
acute or chronic, which results in uremia; but, if the cause be chronic 
contracted kidney, there will be a high arterial pressure, and often 
a strongly beating heart with an accentuated second sound. This 
form with high arterial pressure will often be relieved by full doses 
of nitroglycerin, which not only relieves the tension, but also pro- 
duces an increased renal activity. The urinary examination is of 
the utmost importance, and no surely correct diagnosis can be made 
in any case of suspected kidney trouble until this secretion has been 
examined and found abnormal. (See chapter on the Urine.) 

While headache is far less common as a symptom of diabetes than 
of nephritis, it occurs in the former disease either as a dull pain with 
lassitude and depression of spirits or as violent neuralgia. 

Headache which is constant, although it usually varies in degree, 
may be due to brain tumor, and is one of the most important symp- 
toms to be noted in the diagnosis of a case in which such a lesion is 
suspected. The pain is often worse at night, and is usually more 
severe in persons suffering from tumor of the cerebellum than in 
cases in which the growth is in the cerebrum, probably because 
cerebellar growths often cause effusion which produces pressure 
inside the skull. A tumor of the cerebral cortex, as a rule, produces 
more pain than one in the white matter beneath. Meningeal growths 
are also apt to produce severe headache, but bony tumors of the 
skull often press upon the brain to an extraordinary degree without 
causing any symptoms. 

Headaches due to brain tumor often have exacerbations with a 
regularity suggesting malarial disease, and, conversely, care should 
be taken not to mistake malarial headache for brain tumor. 

After constant headache, the most valuable confirmatory evidence 
of brain tumor is papillitis of the optic nerve, which is present in 
about 80 per cent, of the cases. There may also be vomiting, and 
convulsions if the growth be in the motor cortex. Local paralysis, 
indicating the position of the growth, may be entirely absent, or it 
may exist and yet utterly mislead the physician as to the focal area 
which is diseased, since cases are on record in which, for example, 
a hemiplegia has existed, and at the postmortem examination the 
growth has been found in the frontal lobes. Tumors of the base of 
the brain cause focal symptoms most commonly, and in addition to 



) IE AD ACHE 473 

Unilateral choked disk we find in many such cases ptosis from par- 
alysis of the oculomotor nerve, disturbances in the functions of the 
trifacial nerve in its sensory filaments, so thai painful tic (see chapter 
on the Face and Head) or anesthesia of the face may be present, and 
complete facial (Bell's) palsy may occur. If the hypoglossal nerve 
is affected by the pressure, the tongue is protruded to one side, it 
develops hemiatrophy, and disorders of speech result. Hirt points 
out that a tumor in the anterior fossa is apt to produce paralysis of 
the olfactory and oculomotor nerves and the upper branch of the 
trifacial. A tumor in the pituitary body causes pressure on the 
chiasm with resulting amaurosis, ptosis from oculomotor palsy, 
internal squint from paralysis of the abducens (sixth), and anesthesia 
of the skin and muscles of the eyebrow, forehead, nose, and eye, from 
involvement of the first division of the trifacial. A tumor of the 
middle fossa above the dura causes oculomotor palsy (ptosis . 
patheticus paralysis (downward deviation of eyeball from paralysis 
of the superior oblique), and amaurosis from pressure on the chiasm. 
On the other hand, if it is below the dura, the oculomotor, the 
pathetic, the abducens, and the fifth nerve are paralyzed. When 
tumors occur in the posterior fossa they cause paralysis of the tri- 
facial, facial, auditory, glossopharyngeal, vagus, spinal accessory, 
and abducens, or, in other words, cause anesthesia of the upper part 
of the face, facial paralysis, deafness, loss of taste, irregular cardiac 
action, loss of power in the sternomastoid and trapezius muscles, 
and internal squint. Tumors of the lenticular and caudate nucleus, 
the interior portion of the thalamus, the corpus callosum, the fornix, 
choroid plexus, and of any part of the cerebellum except the vermi- 
form process, may be present without any localizing signs. 

Still more localizing symptoms are early paralysis of the oculo- 
motor nerve from a lesion in the crus, hemianopsia in tumor of 
the occipital lobe, and tonic convulsions with preservation of 
consciousness and a staggering gait in tumor of the vermis of the 
cerebellum. 

Should amaurosis be present, very valuable data as to the position 
of the growth are to be had from a study of the functions of the eye. 
If the pupils react properly to light, this shows that the optic nerves 
and tracts are intact, or, in other words, that the ocular reflex arc is 
perfect, and that the lesion must be in the ocular centres farther 
back. On the other hand, if the reflex is absent the growth probably 
presses on the nerve or tract. (See chapter on the Eye.) 

The failure of a pupillary reaction may, however, depend upon 
amaurosis from lateral hemianopsia, in which case we examine the 
patient for what is known as "Wernicke's sign of hemiopic pupillary 
inaction." This is done by throwing the light by the ophthalmo- 
scope so that it falls upon the blind half of the retina. If the pupil 



474 HEADACHE AND VERTIGO 

does not react, we have in all probability a lesion of the optic tract 
of that side; whereas, if the pupil does react, we have evidence that 
the tract is intact, and there must be a bilateral lesion of the optic 
radiations of the occipital lobes, or in the centre of vision in the 
cortex. (See chapter on the Eye.) 

Other general symptoms of brain tumor are slow breathing, 
particularly when the patient sleeps, a slow pulse, and, as the growth 
increases, symptoms of cerebral compression. It ought to be 
remembered that brain tumor may be closely masked by the results 
of chronic nephritis, for in the latter disease we find headache, local 
palsies or spasms, and, more important than all, an optic papillitis, 
which used to be thought pathognomonic of brain tumor. Albu- 
minuria may be present in both diseases, but tube casts can usually 
be found in renal disease and not in tumor. Both diseases may 
exist side by side. 

Care should be taken in a case of constant and severe headache 
that it be not thought due to brain tumor until the possibility of 
its being caused by a syphilitic arteritis, syphilitic meningitis, or 
syphilitic gumma, is excluded, for mental depression and crashing 
head pains occur in all of these states. This is the more important 
because arteritis is the most common result of syphilis, meningitis 
frequent, and gumma least frequent of all the cerebral complications 
of lues. The differentiation of gummatous tumor from cerebral 
tumor due to other causes may be impossible unless there be a his- 
tory of specific infection or manifestations of syphilis in scars or other 
external signs of syphilis. Improvement in the symptoms under the 
use of iodides and mercury would indicate syphilis rather than a 
growth due to other causes. The presence of optic neuritis would 
indicate tumor or meningitis, and would exclude arteritis; and in 
tumor the pain is apt to be localized, while in arteritis and menin- 
gitis it may be diffuse. The chief symptoms of arteritis are those 
indicating failure of a proper blood supply to the brain, as evidenced 
by giddiness, weakness of groups of muscles, difficulty in speech, 
so that words are dropped out, and, it may be, the presence of symp- 
toms like general paresis. Paralysis, when it develops elsewhere 
than in the ocular muscles, in such cases is usually the result of 
arteritis, since the arteritis results in a thrombus; but when the 
ocular muscles are affected the lesion is probably due to meningitis 
or to nuclear lesions. This development of ocular palsy is of great 
diagnostic significance. (See chapter on Eye and Face and Head.) 
In meningitis, on the other hand, the symptoms are irritative, such 
as spasmodic paralysis and irritative fever. 

The following differential diagnostic table aids in making a diag- 
nosis; but it is to be remembered that all these conditions may be 
very obscure: 



TIE AD AC Ui: 



475 



Syphilitic Arteritis. 
Headache diffuse, often ab- 
sent ; not severe. Not started 
by pressure on cranium. 

Hemiplegia or monoplegia 
frequent. Muscles affected are 
flaccid, and reflexes are ab- 
sent. Paralysis often fleeting 
and limited to a few groups of 
muscles. 

Optic papilla usually normal, 
sometimes syphilitic retinitis 
is present. 

Partial epilepsy rare. 

Aphasia is transitory and in- 
termittent. 

Hallucinations rare. 
Pain in limbs rare and fleet- 
ing. 
Intellectual functions feeble. 
No active delirium. 

Ocular symptoms rare. 



Disorders of sensation are 
fleeting. 

Paralysis of cranial nerves 
not common. 



Temperature may be raised. 



Syphilitic Meningitis. 
Headache diffuse and rarely 
wanting ; sometimes localized. 
Started by pressure or by per- 
cussion on head. Very severe. 

Paralysis, if present, associ- 
ated with rigidity and con- 
tracture, involuntary spasms, 
exaggerated reflexes. Paraly- 
sis more widespread. 

Optic retinitis with marked 
i-ouro-retinitis and abundant 
exudation along the vessels. 

Partial epilepsy common. 

Aphasia less complete but 
more permanent. 

Hallucinations common. 

Severe pain in limbs of cen- 
tral origin. 

Intellectual functions not 
feeble, but may be drowsy. 

Active delirium often present. 

Bitemporal hemianopsia due 
to compression of the chiasm. 
Homonymous hemianopsia. 

Amaurosis from pressure on 
optic tracts. 

Permanent zones of hyper- 
esthesia, anaesthesia, and par- 
esthesia. 

Paralysis ot any cranial 
nerve. 



Temperature quite frequently 
raised. 



Syphilitic Gumma. 
Headache usually localized. 



Distinct focal paralysis com- 
mon. Paralysis associated with 
rigidity and spasm. 



Choked disk often present. 



Hallucinations rare. 



Ocular symptoms of gumma 
involve ocular cranial nerves 
(see text). 



Paralysis of cranial nerves if 
gumma is so placed as to injure 
them. 

Temperature very rarely 
raised. 



In connection with this table, it must be remembered that should 
the arteritis result in degenerative changes descending the pyramidal 
tracts, or in thrombosis with degeneration, the flaccid paralysis char- 
acteristic of arteritis may become spastic. Again, should aneurysm 
arise from the arteritis the pressure upon a cranial nerve may produce 
paralysis, as does meningitis. Then, too, the meningeal symptoms 
may be varied. If the lesion is acute and at the base, there will be 
vertigo, compression of the cranial nerves, polyuria, and bulbar 
phenomena, and finally fatal coma. If it be at the convexity, then 
noisy delirium, convulsions, hallucinations, and paralysis in the 
form of hemiplegia or monoplegia appear. Death comes in coma. 
If it is chronic meningitis of the base, then we may have slowly 
developing alternate hemiplegia, crossed paralysis of the face and 
body, anesthesia of one side of the face, and paralysis of motion on 
the opposite side of the body. If the convexity be affected then 



476 HEADACHE AND VERTIGO 

great irritability of the intellect, sensation, and motion may be 
present. Paralytic strokes are common, but coma is rare. 

Violent headache is the most marked symptom of brain abscess; 
but focal symptoms — that is, localized palsy pointing to the area of 
the abscess — are very often absent, although the localizing symp- 
toms which have just been described as due to tumor may, of 
course, be due to abscess if it is so placed as to press on nerve 
tracts or centres. 

The rises of temperature which frequently occur in cerebral abscess 
are also indicative of the presence of pus, while the more rapid course 
of the disease, often only one or two weeks, points to abscess rather 
than tumor. Further than this, choked disk is rare in abscess and 
common in cases of tumor. 

The difficulty of separating the headache of brain tumor from that 
due to brain abscess is very great, for the symptoms with the head- 
ache are almost if not quite identical in both cases. One of the most 
important of the differential points is the history of an injury to the 
head or of the presence of an infecting focus which could have caused 
cerebral abscess. Another means of aiding diagnosis is to examine 
the blood for leukocytosis. If the white cells are excessive, abscess 
is probably the cause of the illness. 

In some cases of acute cerebral abscess, particularly in children, 
there is a curious tendency to bore the head into the pillow, or, if the 
child is still about the room, the head is rubbed or butted into the 
wall or against the body of the nurse. These symptoms are, however, 
absent in the slow, insidious forms. 

When the physician has made a diagnosis of cerebral abscess 
because of the headache and associated symptoms, he must not be 
misled into a reversal of his diagnosis by marked improvement in 
the patient, who may so far recover as to go back to his occupation, 
for it sometimes happens that a remission or latent period develops 
in the subacute forms of abscess. During this apparent remission, 
however, the temperature is rarely constantly normal, the patient is 
anything but well, and chills may recur. 

Severe headache well diffused over the skull, coming on rather 
rapidly and associated with fever, stiffness of the back of the neck, 
vomiting, photophobia,. delirium, and, finally, stupor and paralysis, 
is probably due to meningitis or to tuberculous meningitis, effusion 
at the base of the brain, or, more rarely, to the onset of a severe attack 
of one of the acute infectious diseases. The differentiation of the 
former from the latter is sometimes difficult, but the finding of some 
local tuberculous focus, the insidious nature of the onset in some 
cases, the family history, and a set of symptoms pointing strongly 
to involvement of the base of the brain indicate that the bacillus 
tuberculosis is the cause of the disease. The fact that these symp- 



HE AD AC 111. 477 

toms are due in sonic cases to the onset of one of the aeute exan- 
themata is established promptly by the appearance of a rash. 

If the disease be tuberculous meningitis, the head pains will often 
be paroxysmal in character, so that the patient will at intervals of 
varying length give vent to sharp cries, evidently due to a sudden 
dart of pain. Vomiting may also be present and ocular symptoms 
develop, such as ptosis, strabismus, and unequal pupils, which have 
a sluggish reaction. The febrile movement will be irregular, now 
high, then very low; the temper peevish, if consciousness is present ; 
and the skin pale and transparent. In the severe and rapid cases of 
tuberculous meningitis marked delirium comes on, the patient pick- 
the bedclothes, and there are tenderness and stiffness of the nape of 
the neck. Pulmonary signs of tuberculous disease are often present . 
and even if absent a focus of tuberculous disease can often be found 
elsewhere. Care must be taken that the case is not mistaken for 
and thought to be typhoid fever, which it may closely resemble in 
its early stages, when headache, malaise, languor, and remitting 
delirium are present. 

In children these symptoms of tuberculous meningitis may be so 
marked as to lead the physician to the diagnosis of this disease 
almost at once. Usually for some two or three weeks before the 
onset of the severe symptoms the child will have been feverish and 
cross. Vomiting of a more or less obstinate form now comes on, 
and constipation is present. The pulse becomes slow and irregular, 
a mild fever is present, and emaciation may be rapid. The general 
nervous state is one of apathy, but finally may be disturbed by the 
sharp hydrocephalic cry. ( )ften the child makes chewing or sucking 
movements. The fact, however, that several other conditions pro- 
duce identical signs in this class of patients renders caution necessary. 
It has just been pointed out that the onset of an infectious disease 
may so result, and it is to be remembered that inflammation of the 
middle ear of an acute type may cause every one of the symptoms just 
described. Such cases are often incorrectly diagnosticated until a 
discharge from the ear with great relief to the patient clears up all 
doubt as to the malady. Then, again, in some cases of croupous 
pneumonia all pulmonary symptoms may be masked in the violence 
of the meningeal manifestations, and, finallv, it is not to be forgotten 
that in some cases of severe gastro-intestinal disorder there may be 
signs of meningeal inflammation, such as coma, squint, convulsions, 
myosis, Cheyne-Stokes breathing, and a depressed fontanelle. 

A valuable symptom of tuberculous meningitis is change in the 
optic disk which may be distinctly swollen. Another ocular symp- 
tom of importance is the presence of tubercle of the choroid. The 
first of these is rarely present in cerebrospinal meningitis, and is 
common in tuberculous meningitis. The second is characteristic 



478 



HEADACHE AND VERTIGO 



of tuberculous meningitis. Another means of diagnosis of tuber- 
culous meningitis is by lumbar puncture. A large, hollow needle is 
inserted at the side of the third or fourth lumbar vertebra in a line 
drawn between the iliac crests across the back. If the needle is in- 
serted properly the subarachnoid fluid speedily escapes from it. 
This fluid, if centrifuged, will, in a large percentage of cases of 
tuberculous meningitis, reveal the presence of tubercle bacilli. 
Another indication that the case is tuberculous is the finding in 
the subarachnoid fluid of an excess of lymphocytes. While this 
excess of lymphocytes is not diagnostic of tuberculous meningitis, it 
is, when taken in connection with the other signs of the disease, of 
great diagnostic importance, and excludes the acute purulent forms 
of meningitis in which an excess of polymorphonuclear cells are 




Fig. 192. — Kernig's sign, showing the strong contraction of the flexors on attempting to 
extend the leg. (After Osier's case.) 

present. Koplik has emphasized the value of percussion of the skull 
in this disease in young children. The child should be upright, 
with the head slightly inclined to one side, and the percussion made 
at the junction of the frontal, parietal, temporal, and great wing of 
the sphenoid bones; in other words, about one and one-quarter 
inches behind the external angular process of the orbit. If, in per- 
cussing this area, a tympanitic note is developed, fluid is present in 
the latter ventricles of the brain, and tuberculous meningitis is prob- 
ably present. Koplik believes that the percussion of the skull in 
the earlier stages of tuberculous meningitis is one of the most valu- 
able aids in diagnosis. 

In some cases of typhoid fever meningeal symptoms develop. In 
some of these the autopsy fails to show any signs of meningeal 
trouble. In others a true meningitis is found. 



HEADACHE 



479 



A valuable sign indicative of meningitis is that of Kernig. The 

patient is placed in a sitting posture at the edge of the bed, with the 
feet on the floor. If meningitis be present, it will be found that the 
leg cannot be extended on the thigh, because of contractures in the 
muscles. If the patient is too ill to sit up, then he should be placed 
on his back, the thigh flexed on the trunk and the leg on the thigh, 
nd an attempt made to straighten the leg, which attempt will fail in 
a large number of cases if meningitis is really present . 

The symptoms of meningitis closely resemble those due to throm- 
bosis of the cerebral sinuses , so closely, indeed, that only the presence 



Communication through parietal 

'oramen with external veins of skidl. 




Tnrenlar 



Internal nasal veins 
communicating thrrfuff 
the foramen c-rcum with 
the sup. long, sinus. 



Fig. 



jugular vein 



Int. jugular 
vein 
193. — Showing the communications existing between the superior longitudinal and 
lateral sinuses and the external veins, indicated in the figure by *. (Lcube.) 



of the typical signs of such occlusions can determine the diagnosis. 
Thus, if the superior longitudinal sinus is affected by thrombosis, 
there may be epistaxis from distention of the nasal veins, and the 
temporal veins will be swollen, and the nearby tissues edematous 
through their close connections with the sinus through the emissary 
veins of Santorini, which escape from the skull by way of the parietal 
foramina (Fig. 193). In children there is usually in such cases 
bulging of the fontanelles and heaviness. Somnolence or delirium 
may be present with many of the characteristic symptoms of menin- 
gitis. This condition usually arises in connection with chronic 



480 HEADACHE AND VERTIGO 

exhausting diseases, such as long-continued diarrhea and the con- 
tinued fevers. 

Thrombosis of the cavernous sinus is usually accompanied by 
quite typical symptoms. There is edema of the eyelids and finally 
of the entire side of the face on the side of the affected sinus, but this 
facial symptom may be absent or very fleeting in its duration. Some- 
times there is exophthalmos, and if the thrombus is septic a phleg- 
monous inflammation of the orbital connective tissue may occur. 
These symptoms are due to the communication between the sinus 
and the ophthalmic veins. Finally, as pointed out in the chapters on 
the Face and Head and on the Eye, paralysis of the oculomotor nerve, 
the ophthalmic branch of the fifth nerve, and of the abducens and 
patheticus may occur, as these nerves pass through the cavernous 
sinus or in its walls. Nearly always thrombosis of the cavernous 
sinus results from some disease processes near by, as in disease of 
the middle ear and mastoid. Sometimes the affection is bilateral. 

If the lateral sinus is affected by thrombosis, there is usually 
marked edema back of the ear, owing to the clot extending to the 
small veins of the scalp, which pass through the mastoid and pos- 
terior condyloid foramina. The external jugular veinpn the affected 
side is partly collapsed, particularly on full inspiration (Gerhardt's 
symptom). Rarely, this vein may be unduly distended (Fig. 194). 
Thrombosis of the lateral sinus occurs far more frequently than that 
of the other sinuses. Suppurative otitis is its most common cause, and 
agonizing earache is, therefore, a symptom often associated with it. 

Not only may cerebral thrombosis present symptoms resembling 
those of meningitis, but in addition those of cerebral abscess. 

Violent headache, with vertigo, staggering, and confusion of 
thought, followed by unconsciousness, may follow meningeal hem- 
orrhage due to disease of the bloodvessels, which are ruptured by 
some strain or by increased blood pressure under the influence of 
stimulants. Hemiplegia or localized spasms may be present. The 
patient may survive several days in severe cases, or may recover if 
the hemorrhage is small; but usually a hemorrhage large enough to 
cause marked symptoms is large enough to cause death. 

The individual affected by meningeal hemorrhage will usually 
be plethoric, and, with the symptoms just described, will suffer from 
photophobia, extreme sensitiveness to the slightest noise, and pain 
radiating down the neck and trunk, which occurs in paroxysms. 
Localized paralysis is rarely present. 

The presence of severe vertical headache in a middle-aged person 
who is insane and who is a male may indicate pachymeningitis 
interna hemorrhagica (hematoma of the dura); but usually the 
insane patient does not complain, and an antemortem diagnosis 
of this state is not made, 



HEADACHE 



481 



Headache resulting from heat-stroke or thermic fever is usually 
the result ofjmeningeal congestion or inflammation, and is one of 
the most annoying symptoms of convalescence. It is apt to be greatly 

increased by moving the head, and is often relieved by venesection. 

The earlier stages of smallpox and pneumonia of the croupous 

type are often periods of violent headache, which symptom in the 



facial vei\% 




Fig. 194. 



Ext. jugul vein 



Communication with veins 
at back of neck 
-Showing the communications existing between the lateral and cavernous sinuses 
and the external veins, indicated m the figure by *. (Leube.) 

former instance decreases with the appearance of the rash, and in 
the case of croupous pneumonia so closely resembles the headache 
and associated symptoms of meningitis that a correct diagnosis, if the 
pulmonary signs are not sought for, may be impossible. In every 
case in which such symptoms occur the lungs should be examined. 
"When headache is present in the course of croupous pneumonia 
it often lasts until crisis, but in some cases ceases by the third day. 
31 



482 HEADACHE AND VERTIGO 

The chest should always be carefully examined in all cases of 
severe headache with fever for signs of pulmonary disease. 

Headache is a constant symptom in many cases of typhoid fever 
in the early stages, but the peculiar tongue (see chapter on Tongue), 
the tendency to diarrhea, the general systemic symptoms, and the 
facies of the patient will usually make its cause clear. More or less 
violent headache is often seen in measles, and depends probably to 
a great extent upon the engorgement of the nasal mucous membrane, 
or, in other words, has the same causative factor as has an acute 
"cold in the head" in producing cephalgalia. 

Gruening is quoted by de Schweinitz as asserting that early morn- 
ing headache is often due to nasal catarrh. This is, of course, only 
true if digestive troubles, which are often due to alcohol, and renal 
disorders are excluded. Severe morning headache, or dull headache 
on first waking up, may be due to nocturnal attacks of epilepsy, of 
which the patient is ignorant. If the tongue is bitten or the bed wet 
with urine, this diagnosis receives strong support. 

Violent headache is often present during the febrile stage of inter- 
mittent fever and is often a complicating symptom of fever of the 
remittent type. In this connection the physician should remember 
that violent neuralgia of the supra-orbital nerve is sometimes due 
to malarial poisoning, and is called "brow ague." f 

Headache is often due to anemia, whether it be the result of hem- 
orrhage or of the deficient formation of blood. The pain is usually 
frontal; there are often giddiness on movement, palpitation of the 
heart, a peculiar sensation in the head, and pallor of the skin. An 
examination of the blood will usually reveal the cause to be in this 
tissue. 

Headache sometimes results from valvular heart disease. This 
in mitral regurgitation is often associated with vertigo, stupor, 
sleepiness, and, as night approaches, a mild delirium may come on. 
Its probable cause is congestion of the brain. 

Rarely intracranial aneurysms produce headache, and when they 
are of the diffuse miliary variety this symptom may be a prodromal 
one before an attack of apoplexy. Large aneurysms may, however, 
exist without severe headache, and the position of the pain in no 
way indicates the seat of the aneurysm, save that aneurysm of the 
basilar artery may cause occipital pain. Auscultation might possibly 
reveal a murmur. 

Headache may also arise from disease of the skull bones, either 
caries, osteitis, or periostitis, which result from injury, infection by 
syphilis or other infecting cause, such as typhoid fever or tubercu- 
losis; but there is nothing diagnostic about the headache in these 
cases save that it is generally most severe in the area involved, and 
pressure over that part may elicit more or less pain or tenderness. 



VERTIGO 4K>> 

Violent neuralgia or shooting headache may be produced by ex- 
posure to cold, with resulting inflammation of the nerve sheath; by 
dental caries, and by middle-ear disease or disease in the external 
auditory canal. 

VERTIGO. 

Vertigo is a condition in which the patient feels as if he were 
losing his equilibrium. Sometimes he feels as if he were whirling 
around from right to left or left to right, sometimes as if falling 
forward or backward, and sometimes he seems stationary, while all 
his surroundings whirl round or rise up to or fall away from him. 
Although vertigo is a symptom which in itself lacks danger, it always 
produces great discomfort, if not fear. Functional vertigo arises 
from the patient being subjected to a whirling motion, from rough 
sea voyages, and from indigestion, deficient circulation, or excessive 
cerebral congestion. Often it is due to cerebral anemia arising from 
excessive hemorrhage. When it arises from indigestion it is prob- 
ably due to reflex irritation, and perhaps to the absorption of toxic 
materials. 

Vertigo as a symptom has a far more serious significance when it 
arises from organic disease. The most common lesions which cause 
it are middle-ear disease, Meniere's disease, tumors of the cerebel- 
lum, of the pons, of the crura cerebri, and the corpora quadrigemina. 
Vertigo also is not only a premonitory sign of an epileptic attack, 
but in the epileptic state called petit mal or minor epilepsy it is 
often the only symptom. In persons with atheromatous arteries it 
is very common, and sometimes it is a persistent symptom for some 
days before an apoplectic seizure. It is also present in disseminated 
sclerosis. Finally, many drugs, such as quinine and the salicylates, 
may produce it. 

As the diagnostic points connected with most of the lesions here 
named are discussed elsewhere in this book, only Meniere's disease 
will be mentioned at this place. In addition to vertigo the character- 
istic symptoms of Meniere's disease are vomiting, noises in the ears, 
and, finally, deafness. The vertigo may be so severe that the patient 
falls to the ground. Aural examinations are usually futile in dis- 
covering any cause. Some authorities believe the disease to be due 
to a neurosis of the vasomotor nerves supplying the semicircular 
canals. 

A form of vertigo unknown in America, the paralyzing vertigo 
of Switzerland, described by Gerlic, is a paroxysmal vertigo with 
great loss of power in the limbs, partial ptosis, and preserved 
consciousness. 



CHAPTER XVI. 

COMA OR UNCONSCIOUSNESS. 

Coma is a condition of unconsciousness or insensibility from which 
the patient can be aroused but partially or not at all, and it may arise 
from injuries to the head, while the patient is in otherwise perfect 
health, which injuries produce laceration of the brain substance, 
cerebral or meningeal hemorrhage, or concussion. Again, it may 
be due to the influence of certain poisons, as alcohol, opium, chloral, 
cannabis indica, very large amounts of the bromides, or poisonous 
doses of other narcotics. Thirdly, it may arise from auto-intoxica- 
tion, as in uremia, resulting from renal disease, in cases of diabetes; 
in cases of profound exhausting disease, like typhoid fever or ulcera- 
tive endocarditis; or from acute yellow atrophy of the liver and 
pernicious malarial fever. Fourth, as a coincident symptom or 
sequel of hemorrhage into the brain (apoplexy), as the result of an 
epileptic attack, of a cerebral embolism or thrombosis, of thrombosis 
of the cerebral sinuses, of cerebral abscess, of pachymeningitis, 
leptomeningitis, or cerebrospinal meningitis, of cerebral syphilis, 
of general paralysis, multiple sclerosis, and heat-stroke. The various 
points in connection with the diagnosis of coma from head injuries 
are to be found in surgical treatises, and the history of a head injury 
or the very presence of any injuries to the head is an important 
point to be sought after in the diagnosis. Care should be taken, 
however, to ascertain that any head injuries found to be present are 
not the result of a fall due to the onset of sudden unconsciousness, 
rather than the cause of the coma. 

The coma of acute alcoholic poisoning is characterized by profound 
insensibility, great muscular relaxation, loss of the ocular reflexes, 
and great fulness of the bloodvessels of the neck and face in the 
early stages, and, finally, by ghastly pallor of the face as the coma 
deepens on the approach of death. The skin is moist and warm at 
first, but afterward becomes cold. The pupils are usually moder- 
ately dilated; the pulse is rapid, at first strong, then more and 
more feeble, and the respiration stertorous and heavy. The 
sphincters, as a rule, are not relaxed, although they may be so in 
rare cases. The bodily temperature in severe alcoholic poisoning 
progressively falls from 1° to 6° F. below normal. 

Alcohol coma is to be separated from that due to opium poisoning 
by the absence of the contracted pupils and slow breathing of the 
latter condition, in addition to the other symptoms named below 



COMA OR UNCONSCIOUSNESS 



485 



in discussing that condition; from coma due to cranial fracture by 
the absence of any history or sign of head injury; 1 from chloral 
poisoning by the history, the greater fall of body temperature, and 
the great feebleness of the heart and respiration produced by chloral. 
It may be impossible to separate alcoholic poisoning from that of 
cannabis indica poisoning except for the fairly strong pulse generally 
found in the latter condition, and the history of the patient having 
taken the hemp or complained of the peculiar sense of prolongation 
of time before the coma came on. 

The symptoms accompanying the coma of opium poisoning are 
heavy sleep, preceding the deep unconsciousness, during which the 
patient can usually be aroused by shouting in his ear or by violent 
shaking, but sinks back into slumber at once on being undisturbed. 
The face is suffused and reddened and may be finally distinctly cyan- 
otic, and the breathing puffing and stertorous. When the patient is 
awakened he breathes more rapidly, and for this reason the duski- 
ness of the face disappears and the normal hue returns. Death 
never occurs in the second stage of opium poisoning from the poison 
alone; but, if disease is present, death may take place at this time. 
The pupils are contracted to pin-points. The third or fatal stage 
emerges from the second by a gradual process, so that no abrupt 
line of separation can be noted. The face becomes at first more 
cyanotic, then pale and livid; the respirations, which have been 
8 to 10 in theminute, are now only 4 or 5; and, finally, such 
prolonged pauses occur that all hope of another respiration is lost 
by the attendant. While the slow breathing is at first deep, it now 
rapidly becomes shallow, and relaxation is present to the greatest 
degree. The skin, previously dry, is wet with the sweat of death; 
the patient is so deeply narcotized that nothing can arouse him, and 
he dies from respiratory failure, although the heart ceases almost 
simultaneously from the asphyxia. The pupils do not dilate in the 
third stage, except in the relaxation of death. 

In view of the frequency with which alcoholic and opium poisoning 
are confused, the following table is appended, which will be found 
of value in making a differential diagnosis as to the condition of the 
patient : 

Opium-poisoning and Alcoholism. 



Opium-poisoning. 

1. Pupils contracted. 

2. Respiration and pulse slow and full. 

3. Face suffused and cyanosed. 

4. Skin warmer than in alcoholic poisoning. 

5. Pulse slow, strong, and full till late in 

poisoning. 



Alcoholism. 

1. Pupils normal or dilated. 

2. Respiration nearly normal ; pulse rapid, 

and finally feeble. 

3. Face may be pallid. 

4. Skin cool, perhaps moist. 

5. Pulse rapid, at first strong, then weak. 



The physician must not forget that a fall from alcoholism may result in a cranial fracture. 



486 COMA OR UNCONSCIOUSNESS 

There is scarcely any difference as to consciousness in these two 
conditions. 

When a poisonous dose of chloral is taken by man the person soon 
falls asleep and then sinks into a deep coma. The respirations 
become at first slow and labored, then shallow and feeble. The 
pulse, at first perhaps a little slowed, soon becomes rapid, thready, 
and shuttle-like, and is finally lost at the wrist. The face is white 
and livid, the forehead and the hands covered with a cold sweat, 
and the pupils, which are at first contracted, soon become widely 
dilated. Absolute muscular relaxation is present, and it is impossible 
to arouse the patient. 

The coma of uremia may come on gradually, but most commonly 
its onset is sudden and follows a uremic convulsion. It possesses 
no diagnostic sign or signs which clearly separate it from the uncon- 
sciousness or coma following epileptic attacks, and, as the uremic 
convulsion is often typically epileptic in character, the differential 
diagnosis is very difficult. An examination of the urine, if it can 
be obtained by the catheter or otherwise, will indicate, but not 
prove, the presence of uremia if albumin be found in either large 
or small amounts, and the presence of very little urine in the bladder, 
indicating anuria, may be of some diagnostic significance. On the 
other hand, if the uremia be due to chronic contracted kidney, the 
urine may be plentiful, the albumin scanty, but the low specific 
gravity be noteworthy. The pulse is usually very slow, often but 
40 to 50, but the arterial tension is high, so that the artery feels 
hard and unyielding. The temperature of the body is usually very 
low in those severe cases which are free from convulsions and have 
a progressively downward course; so low a point as 91° to 95° being 
sometimes reached, at which time the patient is usually moribund 
from collapse. When convulsions are present the temperature may 
rise as high as 108°, and there may be in some cases a severe chill, 
followed by fever, and this again by collapse. The respiration is 
nearly always very deep, and sometimes very much quickened, and 
at times has a peculiar hissing sound. Sometimes the patient may 
purse his lips as if to whistle. Cheyne-Stokes breathing may be 
present. Rarely the breathing is difficult and asthmatic in type 
(uremic asthma) . If a preceding history of prolonged nausea, attacks 
of colliquative diarrhea, and vertiginous symptoms can be discovered 
as having been present prior to unconsciousness, these will add to 
the array of uremic probabilities. The coma of uremia is not neces- 
sarily a fatal symptom. Even in very severe cases remarkable re- 
coveries sometimes occur. 

Coma resulting from diabetes mellitus is of far graver import, as 
it commonly terminates the patient's life. There may not be any 
prodromes, and there may not be any history of an exciting cause 



COMA OR UNCONSCIOUSNE 4^7 

for the coma in a case of diabetes. Sometimes it is provoked in 
patients by severe exercise or great mental strain or emotion. When 
unconsciousness docs not come on at once, the patient, after suffering 
from nausea, headache, and respiratory oppression, suddenly 
becomes anxious, delirious, and violent, then drowsy and deeply 
comatose. The pulse is not particularly noteworthy, but is usually 
full and not very tense. The respirations are deep and often very 
noisy, but at about the normal rate, although sometimes they may 
be rapid in the condition called diabetic dyspnea. The body tem- 
perature falls very greatly, even below 90° F. The respiratory 
changes and those in temperature may, therefore, be very much like 
those of uremia; but in association with the coma of diabetes mellitus 
there are two pathognomonic symptoms: first, the sweet odor of the 
breath, which smells like the aroma of a pear or an apple, or a faint 
odor of chloroform; and, second, the presence of sugar in the urine, 
which secretion becomes dark red on the addition of chloride of iron. 
Testing for acetone usually reveals it in the urine in excess. (See 
chapter on the Urine.) 

Ordinary coma is rare in typhoid fever, and when it occurs is due 
to some complication, such as abscess or effusion at the base of the 
brain or meningitis; it is usually replaced by what is called coma- 
vigil, in which the patient, in a semiconscious state, keeps muttering 
day or night. This is a grave sign. 

The coma of acute yellow afro phi/ of the liver is generally preceded 
by headache, nausea, anorexia, and perhaps fever, followed by ner- 
vous excitement or restlessness, and then mental hebetude, which is 
often accompanied by a noisy delirium which may amount to mania. 
Finally, after several days, coma comes on and gradually becomes 
more and more profound until death takes place. Some of these 
symptoms resemble those of uremia or diabetic poisoning, but the 
coma of acute yellow atrophy has in addition these characteristic 
signs, namely, jaundice, bile-stained urine, marked shrinking of the 
liver dulness, enlargement of the spleen, and hemorrhages into the 
skin, or these effusions may take place into the bowels and stomach. 
The urine is singularly free from urea, but contains leucin and 
tyrosin in large amounts. (See chapter on the Urine for description 
of leucin and tyrosin crystals.) Acute yellow atrophy of the liver is 
so very rare that this disease may be excluded by the law of proba- 
bilities. 

When coma comes on as the result of pernicious malarial infec- 
tion, it is most apt to be ascribed to sunstroke, uremia, or apoplexy, 
for its onset is usually sudden. Only a history of exposure to mala- 
rial influences, the presence of slight jaundice and anemia, and of an 
enlarged spleen will serve to separate it from these conditions, and 
an examination of the blood for the malarial organism may be neces- 



488 



COMA OR UNCONSCIOUSNESS 



sary before a positive differentiation can be made, for the diagnosis 
is by no means easy. 

The coma of apoplexy may be sudden or gradual in its onset ; gen- 
erally it rapidly appears after the first symptoms of cerebral hemor- 
rhage develop. The loss of consciousness may be partial or absolute, 
generally the latter if the leakage from a ruptured vessel be great. 
The respirations become stertorous, generally more rapid than nor- 
mal, and, if a fatal result is in prospect, are rhythmically irregular; 
that is, they are now very slow, then gain in speed gradually until they 
become very fast, then the speed and vigor gradually fall until they 
are as feeble and slow as before (Cheyne-Stokes respiration). The 
history of preceding paralysis on one side of the body, or the presence 
of this loss of power if it can be demonstrated, the unequal pupils, 
the drawing of the face away from the paralyzed side, a strong, 
bounding pulse, and generally raised temperature complete the 
clinical picture of the coma of cerebral hemorrhage. If death does 
not ensue, consciousness may return, and the patient progress to 
recovery; but sometimes after several days of apparent convalescence 
a secondary fatal irritative coma comes on, associated with high 
fever. This is usually of ominous portent and is readily recognized 
because of the history. (See chapters on the Arms and on the Legs 
and on Hemiplegia.) 

The coma of cerebral hemorrhage is unfortunately often taken for 
acute alcoholism, particularly as the latter state often induces the 
hemorrhage. The following table is designed to separate them : 

Acute Alcoholism and Apoplexy. 



Alcoholism. 

1. Pulse rapid, compressible, and weak. 

2. Skin moist, or relaxed and cool. 

3. Bodily temperature lowered. 

4. Pupils equally contracted or dilated ; gen- 

erally dilated. 

5. No hemiplegia. 

6. Breathing not so stertorous nor so one-sided 

in lips. 

7. No facial palsy. 

8. Unconsciousness may not be complete. 



Cerebral Hemorrhage. 

1. Pulse apt to be strong and slow. 

2. Skin hot or dry. 

3. Bodily temperature raised. 

4. Pupils unequal. 

5. Hemiplegia ; one side tossed, the other re- 

maining motionless. 

6. Respiration stertorous, the lips being in- 

flated on one side on expiration. 

7. Facial palsy. 

8. Unconsciousness complete. 



The smell of alcohol in the breath is no guide, as the high arterial 
pressure of acute alcoholism may have caused the rupture of a cere- 
bral bloodvessel. 

Coma due to cerebral softening, following embolism or thrombosis, 
has no signs other than those discussed in the diagnosis of these 
lesions in connection with hemiplegia (which see). Coma due to 
thrombosis of the sinuses of the brain is accompanied by the following 
diagnostic symptoms, namely, irritation or paralysis of the cranial 



COMA OR UNCONSCIOUSNESS 489 

nerves resulting in strabismus, nystagmus, and lockjaw, stiffness of 
the neck, and clonic spasms. If the cavernous sinus is thrombosed, 
there will generally be found stasis of the veins in the eye, which 
means retinal congestion. The eyeball may be protruded, the eyelids 
swollen, and perhaps loss of function in the oculomotor nerve may 
be present, causing ptosis, and, if the abducens is affected, causing 
internal strabismus from paralysis of the external rectus. If the 
transverse sinus is involved, there will probably be edema behind the 
ear, and, if the petrosal or internal jugular be obstructed, the proxi- 
mal part of the vein collapses. Thrombosis of the superior longi- 
tudinal sinus causes epistaxis and engorgement of the temporal veins. 
Thrombosis of any of these sinuses, however, may be present without 
these signs. 

Coma due to subdural hemorrhage (pachymeningitis interna 
hemorrhagica) is peculiar in the fact that its onset is usually very 
slow, and the signs of nervous irritation last a longtime and are quite 
violent, often amounting to epileptic paroxysms. Commonly, too, 
there will be rigidity of one limb, but the cranial nerves usually 
escape. The coma usually follows these signs, and the condition is 
peculiarly common in the chronic insane and in paretic dements. 

Sudden unconsciousness with hemiplegia and vomiting may also 
come on in Raynaud's disease. 

Coma from cerebral abscess is accompanied by symptoms closely 
resembling those of acute meningitis. The patient is dull and de- 
lirious; has headache, fever, and often has a hyperpyrexia. The 
sensibility becomes less and less, and deepens into the coma which 
ends in death if relief is not given. The localizing symptoms of 
paralysis may indicate that a lesion is in a certain part of the brain; 
but generally these signs are absent, because cerebral abscess is 
usually in the frontal lobes. If there is a history of injury, purulent 
otitis, infectious disease involving other parts, such as septicemia 
from wounds or empyema, and if there are vertigo, vomiting, and 
headache, fever, and an absence of choked disk of the optic nerve, 
the diagnosis is probably cerebral abscess; but a long duration of 
months is no sign that it is not abscess, as these cases often run a 
very prolonged course. 

The coma of purulent leftomaringiiis resembles that of abscess in 
many of its associated symptoms; but the intense headache, the 
rapid development of delirium and unconsciousness, the stiffness of 
the neck, the optic neuritis and disturbed movements of the ocular 
muscles, combined with the absence of a history of septic absorption, 
may make a differential diagnosis possible. Purulent leptomenin- 
gitis is rare, but it sometimes occurs in association with croupous 
pneumonia, and the presence of this disease will point to the cause of 
the coma. 



490 COMA OR UNCONSCIOUSNESS 

The coma due to epidemic cerebrospinal meningitis is diagnosti- 
cated by the characteristic rigidity of the neck, excessive headache 
preceding the unconsciousness, the disturbances of the cranial 
nerves producing strabismus, unilateral or bilateral ptosis, nystag- 
mus, impaired pupillary reaction, mydriasis, and myosis. The face 
is often painfully distorted. The presence of an epidemic, of course, 
makes the diagnosis clear. 

It is well to remember that coma may be present from other forms 
of meningitis and arise in several conditions presenting similar 
symptoms, such as pneumonia of the meningeal type, otitic abscess, 
and gastro-enteritis. (See chapter on Headache and Vertigo.) 

Cerebral syphilis may result in the development of coma by pro- 
ducing hemorrhage, embolism, arteritis, tumor of the brain, or almost 
any other lesion, and its diagnosis as the cause of an attack of coma 
is not easy. Of course, a history of syphilitic infection and the 
presence of symptoms of this condition in a patient who is too young 
to have secondary arterial changes from age render the probability 
of syphilis as a cause very great. Scars on the skin (see chapter on 
the Skin) may show specific taint. 

When coma results from general paralysis it usually succeeds the 
peculiar epileptic attacks which come on late in that disease, and the 
history of delusions, tremor of the hands, peculiar speech, loss of the 
reflexes, with earlier milder attacks, like the one before us, combined 
with the age of the patient, render a diagnosis possible. 

Practically identical symptoms may attend the development of 
coma from multiple sclerosis, and without the history of the latter 
affection the diagnosis may be impossible. If this history shows a 
spastic gait and intention tremor, nystagmus, mental weakness, and 
heightened reflexes, the probability of the attack being due to mul- 
tiple sclerosis is increased. 

Coma is sometimes seen as a later manifestation of Addison's 
disease, and it often develops very suddenly. 

Heat-stroke produces coma as one of its almost constant symptoms. 
The history of exposure to heat and the hyperpyrexia are the two 
diagnostic points of importance. (See Fever.) 

Sudden unconsciousness may arise from heart failure due to dis- 
ease or fright ; we call this fainting. Frequent attacks of this char- 
acter should cause the physician to listen to the heart to discover if 
there is valvular disease, particularly aortic stenosis and fatty heart, 
and he should be on the outlook for renal difficulty. Sometimes 
sudden repeated attacks of unconsciousness are due to petit mal or 
minor epilepsy. Coma more or less profound follows attacks of true 
epilepsy. (See next chapter.) 



CHAPTER XVII. 1 

CONVULSIONS OR GENERAL SPASMS. 

Definition of a convulsion — The convulsions of epilepsy in its various forms — 
Of infancy — Of hysteria — Tetanic convulsions — Tetany -Spasms — ( Ihorea. 

A convulsion is a condition in which by reason of sudden tonic 
or clonic contractions of groups of muscles the body in whole or in 
part is thrown into spasmodic movements. Convulsions can be 
divided into those which are clonic or epileptiform and those which 
are tonic or tetanic. Further, it is a general rule that convulsions 
which are epileptiform or clonic in character have their origin in the 
cerebral cortex, while those of the tetanic or rigid type arise from 
excitation of the motor tracts in the spinal cord. The clonic variety 
of convulsions are represented by idiopathic, traumatic, reflex, and 
syphilitic epilepsy, hysterical convulsions of an epileptic type, uremic 
convulsions, and those convulsions which arise from the presence of 
growths or other sources of irritation in the cerebral cortex. ( Certain 
poisons may also rarely produce such attacks, notably lead and 
alcohol, and sometimes malingerers imitate very successfully the 
epileptic paroxysm. 

The convulsion in epilepsy is characterized in some cases by the 
primary appearance of an aura — that is, a sensation in some part of 
the body, which the patient discovers comes on before each convul- 
sion. This aura may be of any character and appear in any part. 
Most commonly it is sensory, and is as if a cloud or wave were passing 
up the body to the head. As the sensation reaches the head the 
patient may utter the peculiar epileptic cry or sigh, and with this 
sound the body becomes rigid from tonic spasm of the muscles. 
This spasm now relaxes for an instant, and then the patient's muscles 
pass into a state of alternate relaxation and contraction which throws 
the patient's body from one place to another. 

The primary tonic spasm of the face produces risus sardonicus in 
some cases: the head is often drawn to one side, the eyes commonly 
turned to the same side, and the lower jaw locked tightly against 
the upper jaw. The arms are strongly flexed at the elbows, the 
hands flexed at the wrists, and the fingers bent into the palms of the 
hands with great force. As a rule, the evidences of the powerful 

1 For local spasms or tremors, see chapters dealing with the Face and Head, Hands and Arms, 
and Feet and Legs. 



492 CONVULSIONS OR GENERAL SPASMS 

flexors overcoming the extensor muscles predominate; but some- 
times the reverse is the case, and forcible, rigid extension of the 
parts affected takes place. The duration of these tonic contrac- 
tions rarely exceeds two minutes, and in most cases is limited to but 
a few seconds. 

It is followed by clonic spasms, already described, which are 
ushered in by more or less violent tossings, but whose onset is fore- 
warned by peculiar vibratory thrills which run through all the 
affected muscles. The eyelids tremble, the body changes its position 
never so slightly, and then, as if the vibrations gained greater and 
greater power with each moment, the fibrillary tremors give way to 
muscular contraction. The expression of the face, which in the 
preceding stage was set and firm, is now constantly changed by the 
movements of the facial muscles ; the jaws, no longer locked together, 
are gnashed and crunched one upon the other; the tongue is alter- 
nately protruded and drawn back, and, as a consequence, is often 
caught between the teeth and lacerated. The excessive movements 
of the muscles of mastication force the increased quantities of liquid 
secreted by the salivary glands from the mouth in the form of froth, 
which is often stained with blood by reason of the h} juries to the 
tongue. The constancy of the convulsive movements now becomes 
less and less marked ; well-developed remissions occur between each 
toss of the body, until the movements cease entirely; but it should 
be constantly borne in mind that the prolongation of the remissions 
does not produce any decrease in the severity of the intervening 
spasm, the final spasm often being even more violent than the first. 

The intense discoloration of the face begins to pass away as soon 
as the remissions, by their length, permit the blood to be oxygenated, 
its disappearance being temporarily arrested by each paroxysm. 
Finally, the spasms having ceased, the patient lies before us relaxed, 
unconscious, and exhausted, and usually passes into a deep sleep or 
coma, which lasts a variable length of time, and from which he cannot 
be aroused, except very rarely, and then with great difficulty. 

When one part of the body is involved in an epileptic paroxysm, 
the rest of it escaping, the condition is called Jacksonian epilepsy. 
By far the most important of its peculiar signs is the character of 
the onset, which always begins, in the typical Jacksonian form, in 
some peripheral portion of the body, and most frequently in the 
muscles of the thumb or hand, so that for the moment the convulsive 
movements are localized. They may remain localized at the point of 
origin, or immediately diffuse themselves over muscle after muscle 
until all the arm, leg, or other groups of muscles are involved. It is 
of the greatest importance, however, that the reader should keep 
the aura of an attack separate in his mind from the onset, remember- 
ing that the term onset is here used by the writer to designate the 



CONVULSIONS OR GENERAL SPASMS 493 

beginning of the period following the aura, if there be one Jack- 
Bonian epilepsy may be of almost any severity. In rare cases only one 
muscle may suffer throughout an entire attack, but in others the 
entire body may be at last convulsed. There may or may not be 
loss of consciousness, its presence or absence being dependent upon 
the seat of the lesion in the brain and the severity of the attack. In 
those instances in which only a few localized muscles are involved 
consciousness is more commonly preserved than lost. 

Typical Jacksonian epilepsy may develop in the course of general 
paresis. 

An epileptiform convulsion may be associated with the onset of 
an apoplexy, and usually indicates that the hemorrhage is in the 
motor cortex. Such an attack is generally Jacksonian in character; 
that is to say, one muscle or a group of muscles is involved, or, if not 
this, the attack is, at most, only unilateral. The cause is made mani- 
fest by the presence of the symptoms of apoplexy as generally seen, 
for there are inequality of the pupils, drawing of the face to one side, 
and a consequent hemiplegia which lasts indefinitely. Of the attack 
itself, it may be said that, so far as the movements are concerned, 
they differ in no way from those of the true Jacksonian epileptic 
seizure; and it should be remembered that hemiplegia often follows 
ordinary idiopathic epilepsy. Such a postepileptic hemiplegia is, 
however, usually fleeting, while that due to hemorrhage is more or 
less permanent. It should be remembered, however, that apoplexy 
may complicate epilepsy, being produced by the convulsion. Then 
again the lesions caused by a hemorrhage may ultimately result in 
epileptiform attacks, although this is certainly rare in adults. In 
some persons the history of this attack is very indistinct, owing to it^ 
occurrence in early life; while in others the paralysis has been so 
slight or temporary as not to bear any relation in the mind of the 
patient with the convulsive seizures following, which in many cases 
do not occur for some time after. The palsy and convulsions are not 
always due to hemorrhage, but to any pathological cerebral change. 
Heart disease, by causing embolism, may bring them on, and syphilis 
and puerperal sepsis may all produce a softening of the cortex, with 
an epileptic state following the paralysis. 

We can very readily divide posthemiplegic epilepsy into two 
classes, for we find that in about one-half of the cases the convulsion 
occurs along with the paralysis and then follows at intervals, while 
in the other half the paralysis is not followed by convulsive seizure.^ 
for weeks, months, or years. 

Posthemiplegic epilepsy may occur at any age, but there can be 
no doubt that it far more commonly occurs in children than in adults. 
In at least two-thirds of the cases the onset is before five years of age, 
and in nearly one-half it is during the first two years of life. 



494 CONVULSIONS OR GENERAL SPASMS 

The frequency with which posthemiplegic epilepsy comes on in 
the hemiplegia of childhood has been very carefully studied, and the 
conclusion reached that its occurrence is quite common. Thus, in 
Osier's cases 20 children out of 97 suffered from it. In the 80 cases 
collected by Gaudard 11 children had hemiplegic epilepsy, and 86 
children out of 100 cases collected by Wallenberg were epileptic after 
hemiplegia. In another series of cases collected by Osier 15 children 
out of 23 were thus affected. (See Cerebral Diplegia.) 

Very interesting results are reached if the statistics of this condition 
are analyzed. Thus, it will be found that in the cases which date 
from infancy females are twice as numerous as males, but in cases 
after five years of age there is no difference between the frequency 
in the two sexes. One of the theories of these infantile cases has been 
that they were produced by the use of instruments during labor, 
and repeated postmortem examinations have confirmed the pos- 
sibility of this occurrence. On the other hand, every obstetrician 
knows that the birth of a boy generally means a more difficult labor 
than that of a girl, owing to the greater size of the head in a male 
child. A priori reasoning would seem to show, therefore, that the 
heads of male children would, accordingly, have instruments applied 
most frequently, and consequently that infantile cerebral trouble 
would be the result more commonly in males than in females; but, 
as has been said, this conclusion is contra-indicated by the facts. 
Another fact of great interest is that the paralysis in the infantile 
cases is more frequently on the left side than the right, but after the 
fifth year it is equally common on both sides. 

The writer has already spoken of the fact that the convulsions 
may occur along with the first attack of paralysis, and continue, or 
that an interval may occur between the attack and the subsequent 
paroxysm. The chronic recurrent fits date from the onset in about 
one-third of the cases, but it is not uncommon for the paralysis to 
occur in infancy and the epilepsy to begin at puberty. It would seem 
that cells injuredin early life may lie undisturbed until the increased 
demands of maturity call them out into diseased action. This pro- 
longed interval occurring so commonly in children separates them 
from adults in this disease, for in the latter class it is very rare for 
the epilepsy to be delayed for more than one year. 

Syphilitic epilepsy is only one of the many nervous affections 
which afflict those who may be so unfortunate as to contract this 
disease. There can be no doubt that syphilis produces epilepsy in 
adults. 

There is also one symptom which may occur early in syphilitic 
epilepsy, or sometimes only late in the disease, namely, repeated 
partial, passing palsies, which while they may be in some cases hyster- 
ical, are in the syphilitic almost pathognomonic of brain involvement 



CONVULSIONS Oil GENERAL SPASMS 195 

— a momentary weakness in one arm; a slight drawing of the face to 
one side, which appears in a few hours; a temporary dragging of 
the toe; a partial aphasia which appears and disappears; a squint 
which tomorrow leaves no trace behind it. (See Syphilitic Arteritis. ) 

It is important to determine whether idiopathic epilepsy can be 
separated from that due to syphilis simply by the symptoms. This 
is very difficult to decide. So far as the convulsion itself is concerned , 
it is not possible to separate them. If, however, we can obtain any 
history, the matter becomes much more simple. 

Fournier, in his lectures on epilepsy, in the Louvain, in Paris, in 
1875, gave a summary of his views as follows: 

1. In the syphilitic epilepsy there is nearly always absence of the 
shrill cry at the onset, so characteristic of the idiopathic variety. 

2. There is frequently paralysis immediately after the attacks. 

3. The seizure is incomplete or unilateral in character. 

4. Attacks constantly increase in severity. 

A therapeutic point, which may be used with the greatest success, 
is the administration of iodide of potassium in large doses. If the 
epilepsy be syphilitic, it will usually become less severe, and enor- 
mous amounts of the drug may be borne with impunity. As much 
as 450 grains in twenty-four hours will often do good. 

Epileptic convulsive disorders may arise owing to the action of a 
very large number of toxic substances, of which only a few will be 
considered here, as an enumeration of all of them is manifestly 
impossible. 

Alcoholic epilepsy consists of two distinct varieties produced by 
over-indulgence in intoxicating drinks. In one of these the convul- 
sions are symptomatic of acute poisoning, and come on during a 
drunken orgy or immediately after a single large draught of liquor. 
In the second variety the convulsion does not originate while there 
is alcohol in the blood, but in the intervals between the attacks of 
delirium tremens resulting from chronic excessive alcoholic indul- 
gence. Under these circumstances the paroxysms are generally 
accompanied by hallucinations or by dementia or imbecility. In 
the alcoholic convulsion the symptoms may closely resemble those 
of true epilepsy, and not rarely the attack is ushered in by headache, 
gastric embarrassment, disorders of vision, and excessive tremors or 
some similar prodrome which may be looked upon as partaking of 
the nature of an aura. As a general rule, these alcoholic convulsions 
occur in paroxysms — two, three, four, or more, one after the other, 
at intervals of a few minutes. Not only may grand mal be closely 
simulated by alcoholic epilepsy, but simple vertigo or true petit mal 
may exist, either alone or associated with major convulsions. Alco- 
holic epilepsy is often associated with hallucinations, especially of 
terror, and not rarely is followed for days by a certain degree of 



49() CONVULSIONS OR GENERAL SPASMS 

mental disturbance. Rather curiously these cerebral disturbances 
result rather in suicidal than homicidal tendencies, which is just the 
reverse of the insanity following simple epilepsy. 

The symptoms of a uremic convulsion will be spoken of further 
when studying its differential diagnosis in connection with epilepsy. 

The diagnosis of lead epilepsy from the idiopathic varieties is 
somewhat difficult, if the patient is seen for the first time during an 
attack; but the ordinary methods of determining chronic lead poison- 
ing are, of course, of equal value here. The blue line on the gums 
may be present, and, if so, the diagnosis is almost certainly lead 
poisoning; but its absence is no proof that lead is not present. The 
administration of iodide of potassium also will so increase the elimi- 
nation of the poison as to benefit the case and render it more easy to 
recover lead from the urine. 

The history of exposure to lead in any form is, of course, exceed- 
ingly valuable evidence, but it should not be forgotten that in many 
cases this history is wanting. Thus, the poison may be derived from 
a hair-dye, or cosmetic, or from water which contains lead from 
pipes, or from an endless line of similar hidden and obscure sources. 
Amaurosis may be present in some cases, or optic neuritis with 
atrophy may occur. Where double wrist-drop is present the diag- 
nosis is much more easy. 

The symptoms of epilepsy due to chronic poisoning by lead are 
chiefly as follows: the man, apparently in his usual health, or who 
has had for a few days a feeling of weight in the head, or headache, 
is suddenly seized with most violent . convulsions, which are often 
fatal, and which during their presence resemble ordinary epilepsy 
so closely as not to be separated from it. They end in coma, and are 
separated from each other by intervals of nervousness and disquiet. 
In some cases one convulsion follows the other so rapidly that death 
ensues from exhaustion, but in much more rare instances the attacks 
may resemble Jacksonian epilepsy very closely, and there may be no 
loss of consciousness. If such a condition occur, it is almost sure to 
be followed by a more violent fit. The attacks are not preceded by 
any aura whatever, but previous to the headache, already mentioned, 
the patient may have had amaurosis, and ophthalmoscopic exami- 
nation of the eyes may show choked disk and neurit : s of the optic 
nerve. As a general rule, such cases are fatal, but they may recover 
under careful treatment. 

It is exceedingly important to differentiate between those convul- 
sions which arise from uremia brought on secondarily by an action of 
lead on the kidneys and those which are due to a direct action on the 
brain. This may be difficult from the mere symptoms presented, 
but there are some points of difference. In the first place, the con- 
vulsion of uremia is, as a general rule, not so violent in its movements 



CONVULSIONS OR GENERAL SPASMS 497 

nor so sudden in its onset. It is generally preceded by a few days of 
somnolence, or weeks of gastric disorder and headache, while lead 
epilepsy is generally sudden or preceded by cephalalgia by only a 
few days or hours. Again, examination of the urine in uremic con- 
vulsions will show a decreased amount of urea in proportion to the 
quantity of urine passed, while in plumbic epilepsy just the reverse 
will be true, unless the kidneys are affected pari passu with the cere- 
brum. If albumin be present, uremia is pointed to; but if the urine 
has a slow specific gravity and is passed in large amounts the indi- 
cations are that there is chronic contracted kidney, which may or 
may not be the cause of the nervous disturbance. 

Malarial epilepsy is an uncommon disorder, even in countries 
and regions which are notoriously malarial, but it has probably 
occurred, particularly in the southern part of the United States and 
in Brazil. The only cases which the writer can find recorded are by 
American or English observers, namely, Jacobi, Payne, and Hamilton. 
The latter gives but a passing glance at the subject, and the articles of 
the others the author has not been able to obtain, so that he knows 
them solely by reputation. In Hamilton's case a young man, who 
had lived for many years in an exceedingly malarious region, had 
more or less periodic epileptic attacks, attended by great preliminary 
rise of temperature and intense congestion of the face and head. 
He was unusually somnolent, and in the intervals frequently suffered 
from facial neuralgia. Change of the place of habitation and the use 
of quinine removed the disease entirely. 

Undoubtedly the most similar convulsive condition that we have 
is that known as hysteria, and the diagnosis of one from the other 
is as difficult in some cases as it is essential and necessary for treat- 
ment and cure. The other conditions with which it might be con- 
fused are uremia, alcoholic epilepsy, tetanus, and syncope. Below 
are arranged all these disorders in a table, which briefly and suc- 
cinctly shows the different points between them, although, of neces- 
sity, it is somewhat arbitrary on account of the lack of space. 

As already stated, in epilepsy the movements are typically at vari- 
ance with those of daily life, while in hysteria they are almost equally 
typical of ordinary muscular contractions, or, in other words, are 
more purposive in character, and frequently there is prolonged tonic 
contraction of the muscles, giving rise to the assumption of positions 
which bear more or less resemblance to normal attitudes. In hysteria , 
also, consciousness is impaired sometimes, but never so completely 
as in true epilepsy. Indeed, most commonly the individual knows 
all that goes on around her, for, while she may give no sign of con- 
sciousness by words or looks during the attack, she may afterward 
be able to narrate all that has occurred. Uess commonly in hysteria, 
a condition known as automatic consciousness exists, in which, during 
32 



498 



CONVULSIONS OR GENERAL SPASMS 



the paroxysm, the patient understands all that is said, but forgets 
everything on the return to quietness. 

Table of Differential Diagnosis of Epilepsy from Hysteria, 1 etc. 



Signs. 


Epilepsy. 


Hysteria. 


Uraemia. 


Petit mal. 


Alcoholic 
epilepsy. 


Tetanus. 


Syncope. 


Apparent 


None. 


Emotion. 


None. 


None. 


None. 


None. 


Mental 


cause. 














shock. 


Aura or 


Generally 


Globus 


Headache, 


Faintness 


Tremors. 


Nervous- 


Not so well 


prodro- 


present, 


hystericus : 


vomiting, 


and dim- 




ness. • 


defined as 


me ta. 


but short. 


palpitat'n ; 
choking. 


and dys- 
pepsia. 
Often 


ness of 
vision. 






in epilepsy. 


Onset. 


Sudden. 


Often 


Sudden. 


Sudden or 


Gradual ; 


Sudden or 






gradual. 


gradual. 




gradual. 


begins 
in jaw. 


gradual 


Scream. 


At onset 


During 


Frequently 


Frequently 


May or may 


None. 


None. 




and sud- 


attack. 


none. 


none. 


not be 








den. 








present. 






Convul- 


First tonic, 


Rigidity 


Rigidity 


No rigidity. 


Movements 


Always 


None. 


sion. 


then 


more pro- 


generally 




more clonic 


tonic. 






clonic. 


nounced, 
with more 

aching. 

People, 


absent. 




than tonic. 






Biting. 


Tongue. 


Tongue. 


None. 


Rarely. 


None. 


None. 






tongue, 
















lips, and 
















hands. 












Micturi- 


Frequent. 


Never. 


Never. 


Rarely, ex- 


Rarely. 


Some- 


Never. 


tion. 








cept when 
bladder is 
affected 




times. 




Defecation. 


Occasion- 
ally. 
Never. 


Never. 


Never. 


Never. 


Rarely. 


Rarely. 


Never. 


Talking. 


Frequent. 


Muttering. 


Never. 


Never. 


Never. 


None. 


Duration. 


A few- 


Generally 


From a 


Momen- 


Maybe 


Hours. 


Indefinite 




minutes. 


many 
minutes. 


minute 
to hours. 


tary. 


prolonged. 




time. 


Conscious- 


Lost. 


Generally 


Lost. 


Not lost 


Lost. 


Pre- 


Lost. 


ness. 




preserved. 




always, but 
clouded. 




served. 




Termina- 


Spontane- 


May be in- 


Spontane- 


Spontane- 


Spontane- 


Sponta- 


Gradual, 


tion. 


ous. 


duced by 
shock, 


ous. 


ous. 


ous. 


neous. 


with no 
somno- 
lence. 



The movements of the hysterical patient after the tonic condition 
has passed away are as clonic as those of the epileptic, but still pos- 
sess some purposive characteristics, and are not so bizarre as are 
those of the true disease. Thus the head, arms, and legs are struck 
with evident endeavor against the floor or surrounding furniture. 
Another point, which, when it occurs, is very distinctive, is the onset, 
toward the close of an hysterical convulsion, of a second stage of 
tonic spasm, such as occurred at the beginning. It will be remem- 
bered that this does not occur in epilepsy, although it must be borne 
in mind that in cases of the "status epilepticus" the rapid onset of 
another attack may show a second tonic stage. This can be sepa- 
rated, however, by the fact that it is followed by clonic movements, 
whereas the secondary tonic stage of hysteria is usually followed by 
relaxation and temporary recovery. 

i This table is taken from the author's essay on Epilepsy, the prize essay of ihe Royal 
Academy of Medicine in Belgium, January, 1889. 



CONVULSIONS OR GENERAL SPASMS }<> ( .) 

In the secondary hysterical tonic contractions emprosthotonos and 
opisthotonos may occur, and are even more rigid in their character 
than they are in the first attack in some cases. Finally, too, in hys- 
teria some peculiar emotional position is often assumed, as of the 
crucifix or of intense grief, or, perhaps, immoderate laughter is 
indulged in, with corresponding movements of the trunk. If the 
patient is quiel at this time, a smile may float across the face, while 
the eyes, with a look of pleasure, pain, or entreaty, may seem to he 
gazing at some object very far off. In some very well-developed 
cases the expression of pleasure is followed by a look of pain, with 
painful movements, or an appearance of intense voluptuous entreaty, 
with sensual venereal desire evidenced by gestures. Great terror 
may be present, and, as the scene constantly changes, the woman is 
now joyous, now mournful, now scolding, now praising her attend- 
ants or herself. Such is the history of a fully developed attack of 
hysteria. 

In France there can be no doubt that the tongue is commonly 
bitten in hysterical convulsions, and that frothing of the mouth is 
frequently present; but in other countries this symptom may be 
regarded as indicative of epilepsy rather than hysteria. Doubtless 
the inexperienced reader will say, upon comparing these symptoms 
with those which were given as occurring in epilepsy proper, that the 
two disorders are easily separated from one another; but the author 
would insist upon the fact that in both cases he has given only the 
most typical characteristics of the diseases, and he repeats that all 
cases are not by any means so well defined. lie would also remind 
the reader that the chief difficulty in making a diagnosis lies in the 
fact that frequently it must be made without any previous history 
of the case, as when a patient is brought into a hospital, in a fit, for 
treatment. When the history is obtainable or when the diagnosis 
can be put off until the case can be studied, the question is more 
easily solved. 

If a large number of patients suffering from these hysterical 
attacks be questioned between times, it will be found that the so- 
called globus hystericus becomes an almost constant precursory symp- 
tom of an attack; and if the relatives be questioned, it will often 
appear that they have noticed that the fall to the floor is more 
gentle than in true epilepsy; but this is not always so by any means. 
Again, the expression of the face in hysteria is, between the attacks, 
often very characteristic, and the surrounding atmosphere of the 
patient seems, even to the inexperienced, to breathe hysteria. Very 
commonly areas of anesthesia and hyperesthesia occur in these 
patients, and are of all degrees of intensity and limitation. Search 
for them generally shows their presence after attacks of convulsions, 
but they may exist from one attack to the other, or develop sponta- 



500 CONVULSIONS OR GENERAL SPASMS 

neously. In nearly all cases these areas are unilateral, and may 
extend entirely over one-half of the body, the line of demarcation of 
the anesthesia or hyperesthesia from the sound area being clearly 
and abruptly defined, generally at the median line of the front and 
back of the trunk. (See chapter on the Skin, that part dealing with 
Anesthesia.) It will be called to mind that such conditions are very 
rare in true epilepsy. Hallucinations are far more common after 
the fit in hysteria than in epilepsy, and sometimes they even occur 
during the attacks. They are always associated with the mental 
state; if terror is present, rats or disgusting objects are seen, and, 
according to Charcot, are generally seen on the side which, during 
the intermissions, is anesthetic. The pupil is more mobile in hysteria 
than in epilepsy, but may be contracted, normal, or widely dilated. 

The following table gives, in as brief a manner as possible, the 
differential diagnosis between epilepsy and hystero-epilepsy, and 
is founded on a lecture by Professor Charcot, delivered at the 
Salpetriere : 



True Epilepsy. 

Aura short. 

Cry is violent. 

Spasms first tonic, then clonic, then followed 
by stertor. 

Sometimes after fit of delirium or violent im- 
pulse or mania. 

Mental power is lost. 

No emotional attitudes. 



Hystero-epilepsy. 

Aura extremely prolonged. 

Cry is more moderate and prolonged. 

Ataxic contractions, extension of limbs, turn- 
ing of head, clonic movements, slight stertor. 

Bizarre contractions, no delirium, may be 
hallucinations. 

Mental power preserved. 

Emotional attitudes. 



A very useful differential point, strongly insisted upon by Charcot 
and Bourneville, is that in true epilepsy there is generally a very 
considerable rise of temperature during an attack, while in hystero- 
epilepsy the temperature remains normal or is only slightly raised. 

In the diagnosis of true epilepsy from convulsions of a hysteroid 
character it is well for the physician to remember that the proportions 
of the two conditions in frequency of occurrence is, according to 
Gowers, 815 to 185 in every 1000 cases. 

The differentiation of epilepsy from uremia is much more readily 
made, for there is usually a previous history of symptoms pointing 
to renal trouble, as, for example, some edema, or somnolence, or 
mental apathy, for some days or hours before the attack. Of course, 
in such cases recourse may be had to the ordinary tests for such con- 
ditions of the urine as are generally found when uremia exists; but 
it is to be remembered that epilepsy and kidney disease may exist 
hand in hand, and that for this reason the prognosis and diagnosis 
are to be carefully formed and given. If in a given case a prolonged 
history of dyspepsia, of frequent vomiting, occasional attacks of 
dyspnea, and failure of general health is found to be present, the 
correct diagnosis probably will be uremia. The preservation or loss 



CONVULSIONS OR GENERAL SPASMS 501 

of consciousness in uremic convulsions is variable. Generally, if the 
convulsion is widespread and severe, the intellection is lost; hut if it 
be only a slight attack, consciousness may be preserved. So long 
ago as 1840 Bright described cases of uremia, on the other hand, in 
which violent convulsions occurred without loss of consciousness, 
and Roberts has reported similar instances. 

Fatal uremia may also occur in a patient whose urine is appar- 
ently normal; and, in cases of chronic contracted kidney, albumin 
may be absent from the urine for long periods of time. The specific 
gravity of the urine should be carefully noted, and in very doubtful 
cases careful estimations of the urea be made. If the specific gravity 
is constantly below 1 .010, the kidney will nearly always be contracted 
unless diabetes insipidus exists. Tests of samples of the urine taken 
from the total daily quantity should always be made. Another 
means of testing the integrity of the kidney is to administer iodide 
of potassium and study its elimination. It is affirmed that, after a 
full dose, this drug can in an hour be readily recognized in the urine 
by adding nitric acid and then starch; but when contracted kidney 
exists the iodine fails to appear or is excreted only in very small 
quantities. A grain of methylene blue may also be used. (See 
chapter on the Urine.) The temperature of the body may also be used 
to differentiate between uremia and epilepsy. In 1865 Kien called 
attention to the fact that even when uremic convulsions are most 
violent they are accompanied by a fall of temperature of as marked 
a character as the rise noted in epilepsy. Since then this has been 
confirmed by Roberts, Ilirtz, Hutchinson, Charcot, Bourneville, 
and Teinurier. 

The diagnosis between puerperal eclampsia and epilepsy consists 
chiefly in the acuteness of the attack, and the fact that with no pre- 
vious convulsive history a woman becomes suddenly convulsed 
during the pregnant or puerperal state. This is not the place for 
a discussion of the identity of uremia and puerperal eclampsia, 
although we believe that uremia is generally responsible for the ner- 
vous disturbance. If the convulsions are uremic, the temperature, 
according to the investigators just quoted, should fall ; and according 
to Bourneville, puerperal convulsions are distinctly separated from 
those of uremia by reason of the fact that the temperature rises with 
great rapidity in the very beginning of the convulsions, and there 
remains with great steadiness. The condition of bodily temperature 
can, therefore, be used to differentiate puerperal eclampsia and 
uremia. 

It is unnecessary to state once more that petit mat is but a variety 
or modification of haut mal. Nevertheless, it is useful to be able to 
separate it somewhat from the more severe form of the disease in 
the attempt to form a prognosis. 



502 CONVULSIONS OR GENERAL SPASMS 

Some suppose that petit mat may be designated as consisting of 
one or two of the chief symptoms of epilepsy proper, and others have 
thought that the preservation of consciousness was the chief dividing 
line between it and fully developed epilepsy. The last idea is cer- 
tainly incorrect, but it is impossible to give any outline which will 
absolutely separate the two conditions, so far as symptoms go. An 
important and useful point, is that, whereas the inhalation of amyl 
nitrite stops true epilepsy, the use of this drug, as a rule, increases 
the severity of an attack of petit mat. 

The separation of syncope from epilepsy is one of the easier tasks 
imposed upon us. The color of the face, the weakened heart beat, 
sudden loss of consciousness, and the general appearance a i# d us here 
very much but it is to be recalled that in "Stokes- Adams disease" 
epileptiform seizures are often present. 

Before closing this portion of this chapter the writer must bring 
forward the points to be used in differentiating epilepsy from those 
attacks simulated by malingerers. Often this is most difficult; and 
it is related by Fournier that, after his expressing an opinion that a 
man could always tell them apart, one of his assistants threw himself 
to the floor on his next visit in a pretended attack, whereupon 

Fournier, completely misled, exclaimed, "Poor M -; he is 

epileptic!" upon which the assistant, smiling, arose to his feet and 
refuted the statement. 

Very serious injuries are sometimes submitted to by these persons 
to carry out their designs. The points to be looked into are: the 
condition of the pupils, which, in the simulated attack, always react 
normally; the corneal reflexes cannot be held back; the color of the 
face is rarely changed; and the thumbs are rarely flexed as they 
should be. Marc has pointed out that in malingerers the bystander 
can readily straighten out the thumbs and that they remain so; 
whereas in epilepsy they instantly become flexed again. 

Suggestions as to movements are sometimes followed by malin- 
gerers, and the convulsant movements themselves generally lack the 
bizarre character so typical of epilepsy. 

If tobacco or ammonia be held to the nose of the fraud, he gen- 
erally is forced to disclose his true nature, but these drugs have no 
effect upon the unconscious epileptic. 

The fact that in malingerers there is no rise of temperature may 
also serve as a differential point. 

Convulsions Appearing in Infants or young children may result 
from injuries to the brain in birth, from the presence of growths, or 
from other distinct cerebral causes, and irritation of the alimentary 
canal. In these cases they may be reflexly produced. 

There is one variety of infantile convulsive seizure due to menin- 
gitis, which is in itself often tuberculous and associated with retraction 



TETANIC CONVULSIONS 503 

of the head and squint; and another variety in which the symptoms 
very closely resemble those due to actual meningeal lesions, hut in 
reality are quite independent of them. This condition has been 
called "pseudomeningitis" or " hydrocephaloid disease," and is 
seen in young infants generally after attacks of severe diarrhea. The 
fontanelle is depressed, the child is somnolent or comatose, and fever 
may or may not be present. The prognosis in the first class of cases 
is very bad. In the second class it is bad enough, but recovery quite 
often occurs if the treatment generally employed in the first class 
is set aside and a highly nutritious and supporting treatmt nt is 
instituted. 

If a child suddenly develops symptoms of acute meningitis, and 
has delirium, rigidity of the neck, and the major manifestations of 
the disease, the lungs should be carefully examined for croupous 
pneumonia, as this disease in children very often causes these cere- 
bral or meningeal symptoms. Even in the adult maniacal delirium 
and rigidity of the neck may be present in croupous pneumonia, 
owing to meningeal involvement. 

Convulsions, which are epileptiform, sometimes occur in the later 
stages of Addison's disease. 

Epileptiform convulsions may come on in adults as the result of 
multiple sclerosis, and they are very commonly seen in sunstroke when 
the patient is first attacked. 

Severe convulsions have been known to follow irrigation of the 
pleural cavity after aspiration, and they may also be svvn in young 
children suffering from whooping-cough at the time of the paroxysm. 

Tetanic Convulsions. — The convulsions which are of spinal origin, 
namely, those that are tetanic, are the result of tetanus or the inges- 
tion of strychnine in poisonous dose, or its fellow ignatia, and some- 
times are due to hysteria. The diagnosis is aided by what has been 
said in the last few pages in respect to the symptoms of hysterical 
convulsions, and finally in those patients that recover by the dis- 
covery of the hysterical stigmata. 

Tetanus convulsions and strychnine poisoning are to be separated 
from one another by the fact that in tetanus the locking of the jaws 
comes first, while in strychnine poisoning it comes last. The convul- 
sions of tetanus rarely, if ever, completely relax, while those of 
strychnine do have periods of complete relaxation. There is a differ- 
ent history in each case: in one, perhaps, of an injury, as of a nail 
run into the foot; in the other, of a dose of poison having been 
swallowed. 

The differential diagnosis between strychnine poisoning and hys- 
terical convulsions is more difficult. The convulsions are rarely so 
persistently tonic in hysteria as in strychnine poisoning, and the 
peculiar expression of the hysterical face is often seen in this 



504 CONVULSIONS OR GENERAL SPASMS 

disease. The history of the patient, if obtainable, will throw much 
light on the case and aid very materially in the separation of the 
two conditions. 

Tetany. — When a patient is seized with sudden and symmetrical 
tonic spasms of the hands, extending to the upper arms and shoulders, 
so that the fingers are flexed at the metacarpophalangeal joints and 
extended in the phalangeal joints, and the lower limb is flexed, while 
the legs are extended and the toes are flexed, the condition is one of 
tetany. (See chapter on the Hands and Arms, " accoucheur's hand.") 
It is most commonly seen in hysterical cases and has no relation to 
true tetanus. Pressure on a nerve trunk or bloodvessel will often 
produce an attack in such persons, and this is sometimes called 
"Trousseau's symptom." The pressure must be applied for several 
minutes in some cases, and the best place to apply it is the bicipital 
sulcus or the crural sulcus. Sometimes pressure on the brachial 
plexus or on the popliteal space will be provocative of an attack. It 
is not a constant symptom, but pathognomonic if found. Another 
equally useful diagnostic sign is called Chvostek's facial symptom. 
This results from the fact that the facial muscles are irritable, so that 
when they are tapped by the finger tip, or a rubber hammer, con- 
traction results. The tapping is usually applied over the zygomatic 
arch in its anterior portion, and this will result in a spasm of the 
upper lid of the eye and the alse nasi. In other cases stroking the area 
over the parotid will have the same effect. The muscles in tetany 
also have an increased electrical excitability (Erb's symptom). 

It is worthy of note that both Trousseau's and Chvostek's symp- 
toms are sometimes met with in rhachitic children, particularly if 
they have craniotabes. (See chapter on the Head.) Laryngismus 
stridulus will often be found associated with tetany and rickets. 

Under the name Escherich's pseudotetanus a curious symptom 
complex characterized by persistent generalized tonic contractions of 
the muscles of the neck, back, legs, and jaw has been described. 
It may occur alone or in association with an acute infection as diph- 
theria. It is not a true tetanus as its name implies and is really 
a form of tetany. 

Convulsions limited to a few muscles or more widespread in char- 
acter may appear as symptoms in acute yellow atrophy of the liver; 
but the peculiar symptoms of this disease render easy the diagnosis 
of their cause. 

Convulsions may also arise from hematoma of the dura mater 
(internal hemorrhagic pachymeningitis), but the diagnosis from 
those due to cerebral hemorrhage is practically impossible. 

Spasms. — General spasms, in distinction from convulsions, are 
represented by chorea in its various forms, and by saltatoric and 
palmic spasm, paramyoclonus multiplex, and the occupation- 



TETANIC CONVULSIONS 505 

neuroses. There are other localized spasms from nervous diseases, 
such as facial spasm and wryneck, athetosis, and posthemiplegic 
chorea. Some of these conditions will be found discussed in the 
chapter on the Hands and Arms and that on the Face and Head. 

When a patient is afflicted more or less constantly and more or 
less universally by disordered, irregular, jerking movements which 
throw the part or parts affected into unusual positions, which are not, 
however, maintained even for a moment, the condition is probably 
chorea minor. Often the speech is seriously disturbed by reason of 
the choreic movements of the lips and tongue or jaws, and some loss 
of power may be manifest in certain muscles. This true chorea or 
St. Vitus' dance may affect the whole body or only one arm or leg, 
but generally it is diffused. Commonly it ceases at night when the 
child sleeps, but it often persists day and night, and then becomes a 
serious malady, because of the exhaustion produced. It often follows 
fright, prolonged bad weather, and other causes which may upset 
the nervous balance of the child. Chorea in childhood is so char- 
acteristic in its manifestations that it can be readily recognized in 
most cases; but it sometimes has to be separated in adults from 
disseminated sclerosis, progressive muscular atrophy, hysteria, and 
Friedreich's ataxia. The movements in disseminated sclerosis are, 
however, fine muscular tremors, instead of minor jerking movements ; 
and there are present nystagmus and scanning speech in sclerosis, but 
not in chorea. Again, in progressive muscular atrophy there is 
fibrillary muscular tremor, but not twitching of a marked form, 
and the muscles are wasted. In hysteria the muscular movements 
are rarely choreic, and the presence of changes in the color fields 
and the other stigmata of hysteria (see chapters on the Skin and on 
the Eye) renders a diagnosis of the latter condition easy. Fried- 
reich's ataxia is to be separated from chorea by the scanning speech, 
scoliosis, slow incoordinate movements, and the family history of 
the disease. 

Rarely when there is some paresis with chorea, the patient may 
present symptoms of acute poliomyelitis; but the paralysis in the 
latter affection is more marked, and there are no movements in the 
affected muscles, such as occur in chorea. 

Chorea insaniens is a violent form of ordinary chorea associated 
with mania, which is not to be confused with choreic movements 
occurring in the choreic insane. 

Choreic movements sometimes come on in the aged, and must be 
separated from paralysis agitans and senile trembling. This is pos- 
sible by the fact that in paralysis agitans the movements are tremors, 
and there is loss of power with the peculiar facial expression (" Park- 
insonian visage") and a hurrying gait (festination). Senile trembling 
is usually an affection limited to the head, and consists in a tremor 



506 CONVULSIONS OR GENERAL SPASMS 

and not in marked twitching. (See chapter on the Hands and 
Arms, part on Tremors.) 

A rare form of chorea has been called Huntingdon's chorea. It 
occurs in adults about the age of thirty to forty years. It is heredi- 
tary; that is, there is generally a history of the same trouble in the 
ancestors of the patient, and finally as it progresses psychical dis- 
turbances ensue. Irregular movements first appear in the hands, 
which movements become markedly incoordinated, the arms are 
thrown about in excessive and rapid jerkings, and when the infection 
involves the legs a characteristic gait is developed of a dancing or 
"hop, skip, and jump" character. Sometimes, early in the malady, 
the movements can be controlled by the will. The face passes through 
slowly formed grimaces, and the gait may be staggering. The speech 
becomes indistinct, and enunciation is not clear. Finally, dementia 
closes the scene. The movements of Huntingdon's chorea are not 
sudden as in true chorea; it is a disease of adult life, and mental 
disturbance is a prominent symptom. These facts separate it from 
ordinary chorea. 

When the patient involuntarily bends over in a profound bow the 
cause of his movements may be rhythmical contraction of his abdomi- 
nal muscles, producing the so-called salaam convulsions or chorea 
major. 

A still more rare malady is electric chorea or "Dubini's disease," 
in which the muscles of the arm and then the leg on the same side 
are affected with a sudden muscular spasm or shock, such as is pro- 
duced by the electrical current. Wasting of the affected muscles, 
loss of faradic irritability, occasional epileptic convulsions, and rarely 
elevation of temperature come on. The disease is a fatal one, and 
generally occurs in malarial regions in Italy. Under the same name 
of electric chorea Bergeron has described a state of rhythmical mus- 
cular spasm which usually ends in recovery. 

When a condition of clonic muscular spasm affecting the trunk, 
limbs, and perhaps the neck is present, the hands and toes being 
uninvolved, as a rule, the possibility of the presence of paramyo- 
clonus multiplex is to be considered. The spasms in this rare disease 
are bilateral and occur at intervals, often only on an attempted 
movement or speech. So violent are the muscular contractions in 
some cases that the patient may be thrown to the ground, or, if in bed, 
to the floor. These movements may vary from 3 or 4 to 120 per 
minute, but are generally about 50 per minute. The symmetrical 
bilateral involvement, the fact that the movements are not choreic 
in character, and that the patient is a male, are to be remembered 
in making the diagnosis. The ultimate prognosis is favorable unless 
the movements are so constant as to cause exhaustion. Care must 
be taken not to confuse hysterical movements with this condition. 



TETANIC CONVULSIONS 507 

The bilateral movements which affect only the larger muscles, and 
the fact that paramyoclonus multiplex is nearly always seen in the 
male, separate it in part from hysteria, while the hysterical stigmata 
when they are present will point to hysteria as the cause of the 
disorder. 

Sometimes a patient will be met with in whom, when he attempts 
to stand, the leg muscles first become rigid and then are thrown into 
violent contractions, which cause him to jump up and down, or he 
may be thrown to the floor. This condition is called saltatoric 
spasm or "jumpers." It is to be separated from the condition of the 
legs seen in lateral sclerosis of the cord by the fact that in the latter 
disease the legs become spastically stiff on attempting to use them, 
from Huntingdon's chorea in that voluntary movements with the 
hands may be performed perfectly, and from chorea minor by the 
absence of small incoordinated twitchings. 

Such a patient will often act on suggestions or in imitation of the 
acts of other persons or of animals. 

Some writers confine the term "saltatoric spasm" to those cases 
which possess no imitative features. In such cases the disease is far 
more moderate in its manifestations. 

Quite distinct from these clonic spasms of the muscles brought 
on by attempted movement is that in which the muscles become 
tonic on attempted movements. At first they are stiff and slow in 
their movements, but ultimately develop a tonic spasm, so that 
walking is at first almost impossible, but the limbs limber up on 
exercise. This is a rare affection, called Thomsen's disease, or one 
of the forms of myotonia congenita. (See chapter on the Feet and 
Legs.) 

Forced gyratory movements of the body are sometimes seen as 
the result of a lesion of the middle peduncle of the cerebellum. 



CHAPTER XVIII. 

HICCOUGH, VOMITING, REGURGITATION, AND THE CHARACTER 

OF THE VOMIT. 

Due to uremia — Cerebral lesions — Intestinal obstruction — Peritonitis — Cholera 
— Gastric disease — Hepatic disease — Poisons — The appearance of vomit. 

HICCOUGH. 

Hiccough or singultus may or may not possess considerable clini- 
cal significance. Often it arises from slight indigestion. In other 
cases it is produced by the drinking of sparkling wines or waters. 
When hiccough becomes persistent it is a symptom to be regarded 
with interest, for if it continues for a long period of time it is usually 
significant of hysteria or uremia, while if it develops in a patient 
exhausted by some prolonged or severe illness it shows deep depres- 
sion of nervous tone, and is itself dangerous because of the exhaustion 
it speedily produces. Sometimes it is said to be an annoying symp- 
tom after passing catheters or bougies in cases of stricture in the 
urethra. Hiccough develops in peritonitis, and is a most distressing 
symptom. It is also seen in cases of intestinal obstruction and when 
abdominal growths are developing. Singultus also takes place in 
some cases of cerebral hemorrhage, in myelitis affecting the upper 
parts of the spinal cord, and in very rare instances because of severe 
mediastinopericarditis involving the phrenic nerve. It also occurs 
as a result of central nervous irritation in persons suffering from 
advanced anemia, and in cases of suppurative hepatitis. 



VOMITING. 

Vomiting is the act by which the contents of the stomach are 
forcibly expelled from this viscus through the cardiac orifice, the 
esophagus, the pharynx, and the mouth. The vomiting centre in the 
medulla oblongata gives rise to the necessary nervous impulses, and 
is provoked to this by direct stimulation or by reflex irritation. Thus 
in uremia the vomiting sometimes encountered is the result of irrita- 
tion of the centre by some unknown poison. When apomorphine is 
given the centre is also stimulated. Centric vomiting is also caused 
by the administration of anesthetics, notably ether and chloroform. 



VOMIT isc 5og 

On the other hand, gastric, intestinal, or other abdominal disorders 
may reflexly produce very persistent emesis, and for these reasons 
vomiting is of considerable diagnostic importance. 

As vomiting is produced by many maladies, it is a symptom fre- 
quently met with. It occurs with a certain degree of constancy as 
a complication or symptom of uremia, diabetes, apoplexy, brain 
tumor, brain abscess, Meniere's disease, tuberculous meningitis, 
hysteria, intestinal obstruction from its various causes, gastric and 
intestinal indigestion, gastritis, gastric ulcer, gastric cancer, peri- 
tonitis, nephritic colic, hepatic jaundice, hepatic colic, in cholera, 
yellow fever, and a host of other ailments. Sometimes the onset of 
one of the acute infectious diseases of childhood is characterized by 
vomiting. Not infrequently this symptom associated with diarrhea 
masks the presence of the real cause of the illness, as in some cases 
of croupous pneumonia. 

The vomiting of uremia may be one of the earliest manifestations 
of renal disease, and its presence, when persistent in the absence of 
local gastric or other causes, should always lead to an examination 
of the urine, since valuable time may be lost if the patient is con- 
sidered to be suffering from some slight indiscretion in diet. Its 
association either as a preceding, concomitant, or consequent symp- 
tom of coma renders a diagnosis of uremia probable, while a history 
of uremic amaurosis, colliquative diarrhea, and failure of the general 
health will be very important points in reaching a decision. No 
pathognomonic symptoms of uremic vomiting exist unless we con- 
sider the urinary evidence a symptom, but in some cases the vomited 
matters smell strongly of carbonate of ammonium, resulting from 
the decomposition of the urea which has been eliminated from the 
blood into the stomach by the gastric mucous membrane. Uremic 
vomiting is, therefore, not only due to centric irritation by a poison 
in the blood, but to irritation of the stomach by the urea which is 
excreted into it. Diabetes comparatively rarely produces vomiting 
by the toxemia which it causes, but in any case the urinary examina- 
tion and polyuria decide the diagnosis. 

When vomiting results from cerebral hemorrhage, embolism, or 
thrombosis, the focal or hemiplegic symptoms characteristic of apo- 
plexy are present. Possibly the vomiting is more indicative of 
hemorrhage than of plugging of the vessel. A sudden attack of 
vomiting in a previously healthy man of advanced years, or in one 
who is young but has a specific history, should raise the question as 
to the possible presence of one of these lesions; provided, of course, 
that ordinary gastric disorder is not present as a cause. 

The vomiting due to cerebral tumor is generally accompanied by 
the characteristic severe and constant headache, vertigo, a slow pulse, 
impaired memory, and sometimes by epileptiform convulsions. 



510 HICCOUGH, VOMITING, REGURGITATION 

Further than this, the important diagnostic ocular symptom called 
"choked disk" of the optic nerve is to be sought for, and if found is 
of great positive value. Tumor of the brain, if near the base, often 
causes, too, involvement of the various cranial nerves. (See chapter 
on the Eye.) The vomiting of cerebral tumor is independent of 
taking food, and commonly comes on early in the morning, thereby 
differing from some of the forms of vomiting due to gastric disorder. 
The vomiting arising from cerebral abscess has symptoms precisely 
like those just named, so that a differential diagnosis is almost impos- 
sible. The history of injury or of an infectious process producing a 
secondary brain abscess may point to this cause of the vomiting: 
the real points of difference are that in abscess choked disk is rarely 
seen, fever is commonly present, and the cranial nerves generally 
escape. When purulent meningitis produces vomiting it may be 
impossible to tell whether this symptom is due to it or to an abscess, 
as the purulent collection may be localized. Vomiting sometimes 
results from profound cerebral anemia of an acute type due to hemor- 
rhage, in fainting or in chronic anemia, as in chlorosis. Generally, 
however, the symptom is only a constant nausea. The presence of 
great pallor and other evidences of anemia aid in the diagnosis, but 
it must not be forgotten that some severe anemias are accompanied 
by febrile movement and by marked choked disk, which should not 
mislead the physician into a diagnosis of cerebral tumor. 

When vomiting is due to cerebellar tumor, the diagnosis is aided 
by the presence of vertigo, the peculiar staggering gait, and finally 
by evidences of choked disk, on ophthalmoscopic examination, with 
disordered vision. 

The vomiting of meningitis is quite frequently an early symptom, 
but it also often occurs later in the disease, and is caused by the 
meningeal irritation, and not by any condition of the stomach, unless 
that viscus has been disordered by the unwise use of drugs. This 
form of vomiting can nearly always be separated from that due to 
other causes by the excessively severe headache, chiefly of an occipi- 
tal type; by the pain in the nape of the neck and in the spine; by 
the rigidity of the dorsal muscles, so that opisthotonos may be caused 
in severe cases; and, finally, by the disordered functions of the 
cranial nerves, as a result of which there are found trouble in the 
oculomotor nerve, strabismus, double or single ptosis, slowly react- 
ing pupils, which may be unequal, nystagmus, and sometimes facial 
contractions due to involvement of the facial nerve. 

Vomiting due to acute miliary tuberculosis often comes on at the 
very onset of the malady, and is associated with obstinate constipa- 
tion, or, on the other hand, active diarrhea; but the fever, the very 
rapid pulse, the wasting of the patient, the possibly present physical 
signs of tuberculosis of the lungs, and, very important, the peculiarly 



VOMITING 



51] 



severe dyspnea, for which no adequate cause can be discovered on 
physical examination, all point to the general infection. If a skilful 
examination of the eye can be made with the ophthalmoscope, the 
choroid may be found to be studded with tubercles. 

The reflex forms of vomiting are very numerous, and depend 
chiefly upon organic and functional disorders of the abdominal 
viscera. In some of these conditions vomiting is of little importance, 
except for its gravity if the patient is exhausted; in other words, 
it is simply a disagreeable symptom. In others the symptom vomit- 
ing is of considerable diagnostic value as indicating the grave mis- 
chief which produces it. One of the most important of the latter 
conditions is intestinal obstruction, whether it arises from intussus- 
ception, constrictions by bands, volvulus, or impactions. 



Middle 

(returning) 

tube. 




Internal 

' < nl< ring) 
tube. 



Fig. 195. — Intussusception. 



In intussusception vomiting is practically a constant symptom, 
occurring with the sudden pain, or, at times, even preceding it. 
In children it continues until shortly before death, and is rarely 
feculent. 

In the adult, and in the chronic form, there may be complete 
absence of vomiting, though this is certainly exceedingly rare. 
Leichtenstern takes exception to the statement that the seat of 
obstruction is indicated by the period at which vomiting is developed. 
The ileum invagination is most frequently accompanied by early 
vomiting, not because of its seat, which is usually but little removed 
from the ileocecal valve, but because it is commonly obstructive. 
The vomiting, both in time of development and in nature, will depend 



512 HICCOUGH, VOMITING, REGURGITATION 

not upon the seat of the trouble, but upon the presence or complete- 
ness of obstruction, and may be early if the obstruction is absolute in 
the sigmoid flexure, and feculent if the occlusion is in the upper part 
of the ileum. 

The pain is usually sudden, violent, diffuse, or, if localized, usually 

centred in the ileocecal or umbilical region. After a few hours in 

children, a much longer interval in the adult, the pain ceases, often 

s suddenly as it commenced, and there is an interval in which there 

little to suggest that the pathological condition still continues. 
This is followed by a return of the pain, the paroxysms becoming 
more violent and prolonged, the intervals less marked as the disease 
progresses, or in the adult, if it passes into the chronic form, and 
intervals even of days may elapse between the paroxysms. The 
pain is frequently accompanied by tenderness, but this is an exceed- 
ingly variable symptom, and at times pressure seems to relieve the 
pain. 

Blood-stained mucous evacuations are a symptom of intestinal 
obstruction which, in children, is rarely wanting. Of 108 cases of 
invagination in the first year of life this symptom was absent in but 
4. It occurs within a few hours of the first attack. At the first 
the discharge is of blood-stained feces ; later, if obstruction is devel- 
oped, of blood and mucus, and is usually exceedingly offensive. In 
children diarrhea is common throughout the whole course of the 
case. At times, following complete constipation and feculent vomit- 
ing, there will suddenly appear copious evacuations from the bowel, 
mingled with blood, in which may be found evidences of the necrosed 
intussusceptum. Where this slough is extensive it may be lodged in a 
lower portion of the bowel and cause fatal obstruction. 1 

In connection with the mucosanguinolent evacuations the tenes- 
mus or straining is a symptom so common that it is of some diag- 
nostic import. That it is not dependent upon the character of the 
evacuation is shown by the fact that it is present in cases of complete 
obstruction. Brinton has shown that this symptom is seldom 
developed except in the ileocecal and colon invaginations. 

A much rarer condition, and one which Leichtenstern ascribes to 
the secondary effect of intense tenesmus, is a patulous condition of 
the anus due to paralysis and dependent upon invagination of the 
descending colon and rectum. This is never produced by invagina- 
tion of the ileum. 

Leichtenstern's statistics show that a tumor can be felt either 
through the parietes or by rectal examination in 52 per cent, of all 
cases. In the first year of life this most important diagnostic sign 
was present in 63 per cent. The tumor is usually felt in the left 

i For much information on the subject of intestional obstruction, see the Fiske Fund Prize 
Essay of the Rhode Island Medical Society for 1899, by Dr. Edward Martin and the author, 



VOMITING 513 

iliac region, or by the finger passed into the anus. The ileocecal 
invagination is most frequently accompanied by demonstrable tumor; 
the ileum invagination exhibits this symptom with less frequency. 

Many authors have noted that the tumor varies in size and con- 
sistency from time to time, now, during an acute paroxysm of pain, 
being hard, knotty, and plainly perceptible, shortly afterward eluding 
the most careful search. Duchaussoy has described two distinct 
movements which can often be perceived in the tumor, namely, the; 
erectile and the vermicular motion. 

Distention of the abdomen is not of great significance, because it 
is often absent. In children especially it may not appear at all, or 
may appear only just before death. In adults, in whom obstruction 
is more common, it may become as well marked as in obstruction 
from any other cause. 

In the chronic form of invagination the symptoms are less violent 
in onset; there may be nothing more characteristic of the attack 
than recurring paroxysms of pain, meteorism, and obstruction, witli 
symptoms of intestinal stricture constantly manifesting themselves. 
These cases terminate either in cure by reduction or by extrusion of 
a slough, or perish from exhaustion, inanition, or in the course of 
an acute attack. In over one-half of the recorded cases a correct 
diagnosis was not made. 

The additional symptoms upon which a diagnosis of vomiting 
from intussusception is to be based are the acute onset of colicky 
pain, and its intermittent character; passages from the bowels con- 
taining blood and mucus; the presence of tumor, commonly in the 
left iliac region, or felt through the anus, varying in size and con- 
sistency from time to time, with an erectile or vermiform motion; 
and the ordinary obstruction symptoms. The diagnosis is further 
confirmed if there are present violent peristalsis and tenesmus, and 
if these symptoms occur in an infant. 

According to Leichtenstern, Bryant, and others, 40 per cent, of 
all cases of intestinal obstruction are due to intussusception, and 
this condition is most common in the first year of life, after which 
it becomes more and more rare until the fortieth or fiftieth year, 
when it increases in frequency. The prognosis is bad, the mortality 
varying from 73 to 90 per cent, unless early surgical relief is given. 

Internal strangulation by bands occurs in from 25 to 30 per cent, 
of the cases of obstruction of the intestine, and affects males most 
commonly between twenty and forty years of age. In 133 out of 151 
cases the small intestine was involved. The typical symptoms are 
as follows : 

1. Sudden, agonizing pain, constant, and located about the um- 
bilicus, with paroxysmal increments. 

2. A rapid, weak pulse and subnormal temperature. This is 

33 



514 HICCOUGH, VOMITING, REGURGITATION 

nearly constant in the early stages of the attack; later on, when 
local or general peritonitis develops, the temperature and pulse may 
assume the features characteristic of inflammation. 

3. Vomiting. First of the contents of the stomach, then of bile, 
and, finally, in a large percentage of cases, of feculent matter. The 
feculent vomiting rarely appears before the third day, and in cases 
running a very acute course death may ensue before this symptom 
has time to develop. The vomiting is constant and gives no relief 
to the patient. 

4. Constipation. Exceptionally there may be one or two passages 
representing the contents of the bowel below the seat of obstruction ; 
after that the constipation is absolute, not even flatus passing by 
the anus. Treves has suggested that the evacuations sometimes 
observed toward the termination of the case, and not due to the relief 
of obstruction, may be dependent upon the beginning of peritonitis. 

5. Tympanitic distention. Where there is a large segment of 
gut involved in the strangulation its early distention may give rise 
to a localized abdominal enlargement, which is exceedingly sugges- 
tive as to the cause of the attack. In general, the meteorism is not 
marked except when peritonitis supervenes. 

Since in the large majority of cases the obstruction is localized in 
the lower portion of the small intestine, the primary distention will 
be observed in the middle abdominal region — i. e., the epigastric, 
umbilical, and hypogastric areas. Laugier claims by this symptom 
to locate the obstruction with some certainty. 

The violent peristalsis and repeated vomiting prevent the extreme 
meteorism characteristic of intestinal paralysis. 

6. Localized tenderness and percussion dulness. When present 
these signs are of exceedingly great importance, since they denote 
the position of the strangulated bowel. 

Exceptionally a tumor may be felt, formed by the congested gut 
or the matting together of the intestinal coils. 

The urine is diminished in quantity and may be suppressed. In 
acute strangulation it commonly contains albumin, and it is stated 
that this is of diagnostic value. 

In this connection the history is of great importance. 

Other congenital deformities would suggest the possibility of 
Meckel's diverticulum as a cause. 

A preceding typhlitis, pelvic peritonitis, or severe abdominal trau- 
matism would respectively assign an adherent vermiform appendix, 
peritoneal bands, or rents in the omentum or mesentery as the causa- 
tive agents in the production of the symptoms. 

The age of the patient should also be considered, since this form 
of obstruction usually occurs between the twentieth and fortieth 
vears. 



VOMIT IXC 



DlO 



The sudden onset of violent, persistent pain, subnormal tempera- 
ture, and frequent pulse, the obstinate, absolute constipation, the 
persistent, repeated vomiting, becoming fecal, and the rapid course 
of the disease, all point to internal strangulation. 

Auscultation of the abdomen is at times of value, a sound com- 
pared to the click of the water-hammer being heard most distinctly 
at the point of obstruction. 

Palpation and percussion should not be omitted, as thereby the 
seat of obstruction has been distinctly located. 

Volvulus is the most frequent form of intestinal obstruction after 
intussusception and that due to strangulation. Vomiting occurs, 
but is not so constant a symptom as in those forms first named. 
Thus it occurred in from 8 per cent, in Brinton's statistics to 2.5 per 
cent, in those of Treves, and 4 per cent, in Martin's and the author's. 
It is nearly always seen in men in middle life. The vomiting is rarely 
fecal, is very slight in many cases, and sometimes does not appear 
at all. 

Vomiting, on the other hand, is quite commonly seen in the cases of 
obstruction from impaction or obstruction from foreign bodies. 
The distention is slight, the amount of systemic shock far less 
than in other forms of obstruction, and the duration of the attack 
somewhat longer than usually obtains in this class of affections. 
The symptoms of obstruction are frequently only partial, the vomit- 
ing being moderate in amount and not stercoraceous, the constipation 
not being absolute. 

Except in the case of enteroliths and very large foreign bodies a 
tumor can rarely be felt. 

It is often impossible to diagnosticate this form of obstruction from 
that depending upon a narrowing of the lumen of the bowel, such as 
is produced by cancer or stricture. The previous history is always 
of great importance. 

In this connection it is to be remembered that hemorrhagic infarc- 
tion of the intestine may produce symptoms similar to those just 
described, namely, pain in the region of the navel or more generally 
throughout the belly, fecal vomiting, diarrhea, and bloody stools. 
Actual obstruction may be present. Search should be made for a 
source from which an embolus may arise, as, for example, valvular 
cardiac disease, and if this is found the likelihood of infarction being 
present is increased. 

When persistent vomiting develops in an infant during the first 
few weeks of life and no error in diet can account for the symptom, 
the physician should consider the possibility of the presence of 
congenital hypertrophic stenosis of the pylorus. At first the symp- 
tom may be present only after food is taken and the quantity ejected 
may be small or it may be greater in amount than the food recently 



516 HICCOUGH, VOMITING, REGURGITATION 

swallowed, indicating retention in the stomach of a former meal. 
Bile is never present in the vomit. In a few days the stomach 
becomes remarkably intolerant of food and the vomiting may be pro- 
jectile in character. Rapid emaciation takes place and the physician 
may on palpation find a tumor at the pylorus. On inspection waves 
of contraction in the walls of the stomach may be seen passing from 
left to right. 

When vomiting arises from general peritonitis it is often one of the 
earliest symptoms of the malady. It is almost always present, and is 
often a very severe symptom, and is associated w T ith or replaced by a 
constant retching, which adds to the exhaustion of the patient. At 
first it may only follow the swallowing of food, but often it occurs 
without such a cause, and after the stomach is emptied of its ordinary 
contents glairy, watery mucus is expelled, which is often of a distinct, 
greenish tint. The great tenderness of the belly in acute peritonitis, 
the moderate fever, the rapid pulse, the anxious face, and the cold 
skin as collapse approaches, all render the diagnosis easy; but it is to 
be remembered that the distention of the belly by an overfilled blad- 
der or pregnant uterus may mislead the physician into thinking that 
peritonitis is present because of the swelling, the pain, and the vomit- 
ing. Vomiting is not a severe symptom of appendicitis unless the 
peritoneum has become involved in the inflammatory process, 
although it may occur once or twice when the pain in the appendix 
is most severe. The localization of the symptoms in the neighbor- 
hood of the appendix makes the diagnosis possible. (See chapter 
on the Abdomen.) 

When vomiting occurs in typhoid fever it is usually a symptom of 
bad feeding or imperfect digestion, and is rarely of grave importance 
except under two conditions. The first of these is when it occurs 
as a result and symptom of intestinal perforation, an accident com- 
monly seen late in the disease; and, second, when it takes place as 
an obstinate and exhausting symptom after the fever has practically 
passed by, from unknown causes, probably toxic in character. The 
symptoms of perforation other than vomiting can be found in the 
chapter on the Abdomen and Abdominal Viscera. 

Vomiting as a symptom of cholera is accompanied by serous 
diarrhea of profuse character, by the development of collapse, cramps 
in the muscles, anuria, and great circulatory failure. It should be 
separated from the vomiting due to cholera morbus or severe indiges- 
tion, antimonial poisoning, and arsenical poisoning. Cholera morbus 
is to be separated from cholera, first, by the absence of the comma 
bacillus in the stools; second, by the fact that there is a history of 
exposure to cold or damp, or bad food; third, by the absence of an 
epidemic; and, fourth, by the fact that its manifestations are milder. 

No one can be skilful enough to separate symptoms of poisoning 



VOMITING 517 

by antimony from those due to eholera, for they are identical in 
every way. Nothing but the history of the ingestion of the poison 
and the discovery of antimony in the excretions can prove the case to 
be one of antimonial poisoning, particularly if an epidemic of cholera 
is present. 

In arsenical poisoning the association of vomiting with bloody 
stools separates the symptoms from those of cholera. 

Vomiting is often a very severe and early symptom of eholera 
infantum (see chapters on the Abdomen and on Bowels and Fc< 
and it occurs in attacks of true dysentery as a common symptom, 
when its underlying cause is readily discovered. (See Abdomen.) 

The diseases of the stomach causing vomiting are cancer, ulcer, 
gastritis, catarrh (acute and chronic), true gastritis, and dilatation. 

The vomiting of gastric cancer at first consists in the expulsion 
from the stomach of its contents — mixed particles of food, mucus, 
water, and sometimes bile. The vomit may be tasteless or sour from 
fermentation, and may have an offensive odor from similar causes. 
Often it contains blood, either in bright-red streaks or as a brownish- 
red fluid, or in similarly colored clots, which may be brown when 
they have been in the stomach for some time. Often the exuded 
blood, changed by mixture with the stomach contents, looks like 
coffee grounds, producing ''coffee-ground vomit." This coffee- 
ground vomit is not pathognomonic of gastric cancer, but is very 
characteristic of this disease. Microscopically the vomited materials 
are seen to consist of panicles of food, yeast cells, cocci, and broken- 
down blood corpuscles. (For the other symptoms of gastric cancer, 
see chapter on the Abdomen.) 

Coffee-ground vomit is also sometimes seen in cases of locomotor 
ataxia following a gastric crisis. Roux asserts that overdoses of 
iodide of potassium may produce a gastric crisis in locomotor ataxia 
by irritating the stomach. 

Vomiting due to gastric ulcer is preceded by pain, and is generally 
brought on by taking food, and so occurs soon after eating. The 
food is, therefore, only slightly digested, and evidences of fermenta- 
tion are absent to a great extent. If blood is present, it is nearly 
always bright red and in considerable quantity, and indicates that a 
hemorrhage has recently taken place from the surface of an ulcer. 
Very profuse hemorrhages into the stomach may cause vomiting by 
irritating and distending this viscus. The history of vomiting after 
eating, the presence of blood in the vomit, the pain in the stomach, 
the age of the patient (generally twenty to thirty years), the sex 
(generally female), and the hyperchloric acidity, combined with 
the other symptoms (see chapter on the Abdomen), complete the 
diagnostic array of facts. 

There are, however, other causes of vomiting of blood or hema- 



518 HICCOUGH, VOMITING, REGURGITATION 

temesis than gastric ulcer and cancer. Thus, it occurs from obstruc- 
tion to the portal circulation from hepatic cirrhosis, and from growths 
and splenic affections which result in varicosity of the bloodvessels 
of the stomach. Hematemesis also follows severe blows, kicks, and 
other injuries to the epigastrium. Sometimes it takes place in cases 
of heart disease in which there has resulted hepatic engorgement 
with secondary gastric congestion, and it may be developed in small 
degree by any form of violent vomiting which strains the stomach, 
particularly if an irritant substance has already destroyed the 
mucous membrane. Again, hematemesis is seen in scurvy, typhus, 
yellow fever, and acute yellow atrophy of the liver, as a result of 
breaking down or destruction of the coats of the vessels. Sometimes 
it is seen in cases of dengue, in influenza of the epidemic type, and 
in relapsing fever. Hematemesis may also occur in purpura hemor- 
rhagica, in hemophilia, and possibly as vicarious menstruation. 
In malarial fever of a severe character the dark-colored vomit is 
generally due to bile, but it may be due to exuded blood. Such a 
case is reported by Boon as occurring in a child. 

Care should always be taken that the physician is not misled by 
the vomiting of swallowed blood into a diagnosis of gastric hemor- 
rhage from any of the causes just named. It may enter into the 
stomach from the pharynx, as after epistaxis, or blood may be swal- 
lowed by a malingerer. Hematemesis is to be separated from hemop- 
tysis by the fact that in the latter there are physical signs in the 
lungs, the sputum is frothy and bloody, there is absence of retching 
or vomiting movements, and the blood is brighter red in hemoptysis 
than in hematemesis, as a rule. 

Under the name of melena neonatorum there is a condition of hema- 
temesis occurring in children within the first few days or weeks of 
life. This condition has been thought by Leube to be due to gastric 
and duodenal ulcers, and his views are indorsed by Buhl and Huhn, 
Spiegelberg, Binz, and Landau. In one of the latter's cases throm- 
bosis of the umbilical vein was present, and it has been thought 
that when expansion of the chest takes place in the newborn child 
small clots may escape from this vessel through the ductus arteriosus 
into the descending aorta and gastric arteries, and thus cause an 
ulcer of the stomach by embolism. 

The vomiting of acute gastric catarrh is generally seen in children, 
and is often preceded by great nausea. The contents of the stomach 
are first gotten rid of, then mucus, water, and bile may be ejected, 
and finally exhausting retching ensues if the attack is severe. The 
tongue in such cases is coated and dotted with red spots from the 
enlarged fungiform papillae, and the epigastrium is tender on pres- 
sure. There may or may not be fever and looseness of the bowels. 
The attack usually follows indiscretions in diet or exposure to cold. 



vomitisc 5lg 

Vomiting from chronic gastric catarrh is usually a condition met 
with in adults, and when seen in the male is most frequently the 
result of a frequent use of alcoholic beverages to excess. In women 
it often develops from excessive tea drinking associated with errors 
in diet. When due to alcoholism, the vomiting is often present only 
in the morning before or after taking food, and then is called the 
"morning vomiting of drunkards." (See chapter on the Tongue.) 

Vomiting due to true gastritis or inflammation of the stomach in 
its deeper layers is very rare, except as a result of the ingestion of an 
irritant poison or hot liquid. 

Perhaps the vomiting occurring in dilatation of the stomach is 
more typical in its character than any other. This act is often a 
prominent symptom of gastric ectasy, the matters vomited being 
often greenish and extremely fetid, and nearly always profuse in 
amount. Examination of the ejecta will generally show food swal- 
lowed days before, owing to the imperfect digestive action of the 
stomach, and this very inability of the stomach to act on the food 
generally gives, for a long period of time, a sense of weight and 
fulness often amounting to pain, and complained of bitterly. There 
is tenderness over the epigastrium on pressure, and the displacement 
produced by the palpation often brings on either acid or yeasty eruc- 
tations or even the vomiting already named. Nausea preceding the 
vomiting is by no means common, there being simply a gusli of foul 
liquids from the mouth. After such an occurrence the vomiting 
fails to recur for from twenty-four to forty-eight hours, or perhaps 
for a week — i. e., until the viscus becomes overladen once more. 
The fluids which are given off on eructation are exceedingly acrid, 
nauseous, and bitter. Sometimes they are offensive, but more rarely 
odorless. The reaction of the vomit is almost always acid, lactic. 
and butyric being the acids most commonly found, but the normal 
hydrochloric acid is usually absent. Fibers of meat or masses of 
semi-digested and semi-decomposed food can be seen by the naked 
eye or under the microscope, and sarcimv and many forms of bacteria 
swarm in the mass. Particular search should be made for the yeast 
fungus, Torula cerevisiae, the presence of which is a certain evidence 
of active fermentation. 

(For further information in regard to the symptoms of gastric 
dilatation, see the chapter on the Abdomen.) 

Vomiting due to gastric dilatation should not at once lead the 
physician into a diagnosis of stenosis of the pylorus from growth or 
constrictions in this part of the stomach, or from innate feebleness 
of the gastric walls, for similar conditions may follow growths of 
the pancreas, which by pressure occlude the pyloric opening (see 
chapter on the Abdomen). 

Sarcinse ventriculi are found not only in the frothy, dirty looking 



520 HICCOUGH, VOMITING, REGURGITATION 

vomit of gastric dilatation, but in that of chronic gastric catarrh, 
cancer, and ulcer of the stomach. If iodine or iodide of potassium 
is added to the vomit, the sarcinse become mahogany red or brown, 
and are easily recognized, occurring in squares which are separated 
by dividing lines (Fig. 196). 

Vomiting also arises from neurosis of the stomach in several forms. 
Thus it is frequently seen in hysteria, in neurasthenia, pregnancy, 
and sometimes occurs in the form of what Gee has called " cyclical 
vomiting." It also comes on in association with gastric crises in 
locomotor ataxia. The vomiting of hysteria is generally characterized 
by its persistent character, often lasting for months, and yet the 
patient often maintains her normal weight to a surprising degree, 
either because the food which is taken is only vomited in small part 
or because she surreptitiously obtains food when her attendants do 
not know it, which she retains. It is generally associated with so 
many of the hysterical stigmata as to be readily diagnosticated. The 
vomiting of neurasthenia is seen in both sexes, and is particularly apt 




O 

FtG. 196. — Sarcinse ventriculi, with starch granules and oil globules, from vomited matters. 

(Otto Funke.) 

to follow any nervous muscular exertion. Thus in one case of the 
writer's, even a short railroad journey taken by an overworked man 
produced attacks of spinal tenderness with vomiting which lasted 
several days. In some neurotic cases the vomiting takes place as 
soon as the food is swallowed. The vomiting of pregnancy is usually 
a morning vomiting, though it may persist all through the day. It 
has no particular diagnostic features in itself, save that there are 
rarely any signs of gastric indigestion. The presence of pregnancy, 
of course, makes the diagnosis clear; and in such cases the physician 
should always examine the urine, since although the ordinary vomit- 
ing of pregnancy is a symptom of the first few months, that occur- 
ring later on may indicate grave renal complications. (See Uremia, 
in chapter on Coma and in chapter on Convulsions.) 

The cyclical vomiting already mentioned is generally seen in chil- 
dren, and is of rare occurrence. It is characterized by attacks of 
vomiting recurring after intervals of uncertain length, during which 
the patient may seem entirely well. The attack may last from a few 



VOMITING 521 

hours to a few days. There are often pain in the epigastrium and 
constipation. Sometimes retching is the main symptom. It is 
generally seen in neurotic patients and is probably a form of acid 
intoxication. 

In acute pancreatitis there is colicky pain in the epigastrium, 
deeply seated and extending to the right shoulder and back, and 
great restlessness, precordial distress, dyspnea, and faintness are 
present. The matters vomited are greenish, clear, and viscid, and 
the efforts at vomiting increase the pain. There is no jaundice, 
but death soon comes to the relief of the patient. 

As an early diagnosis of acute pancreatitis may permit surgical 
interference, with possible recovery of the patient, the diagnosis is 
important. The mistake commonly made is to consider the case one 
of intestinal obstruction. 

Vomiting of a peculiar character is always present in phosphorus 
poisoning. The symptoms associated with ingestion of the poison 
may not come on for some hours. At the end of that time the peculiar 
taste of phosphorus may be noticed in the mouth, the breath is heavily 
laden with its odor, and burning pain in the esophagus, stomach, and 
abdomen ensues. Vomiting and purging now assert themselves, 
and the matters vomited and those passed from the bowels may be 
luminous in the dark, owing to the presence of free phosphorus. 
The vomit is at first made up of food, then mucus, then bile, then 
perhaps blood. All the symptoms of a mild gastro-enteritis may 
develop, but it is to be noted that constipation of an obstinate type 
may replace the purging. Very soon the liver increases in size, and 
gives rise to general hypochondriac pain and tenderness, as well as 
local swelling. At the end of twenty-four hours, or perhaps after 
the second day, a cessation in the symptoms occurs, and, if the 
physician be not on his guard, this will lead him to a hopeful prog- 
nosis. In the course of a few hours jaundice begins in the conjunctiva 
and then extends over the entire body. With the onset of jaundice 
the vomiting and pain return with renewed vigor. The matters 
vomited are often the color of "coffee grounds," due to exuded and 
altered blood. The bowels are absolutely confined, or the few hard 
masses passed are white and clay-like, because of the absence of 
biliary coloring matter. There is no bile in the vomit in this stage, 
because the hepatic ducts have been closed by the inflammation set 
up in the liver. After this nervous symptoms ensue. Muscular 
twitchings, headache, vertigo, wild delirium, erotic convulsions, and, 
finally, unconsciousness and death occur. Sometimes the convulsions 
occur just before dissolution. Even if the patient survive the acute 
stage, he generally dies of the changes produced in his vital organs, 
which consist in widespread fatty degeneration, even in the acute 
stages. Atrophy of the liver, destruction of the gastric tubules, 



522 HICCOUGH, VOMITING, REGURGITATION 

pancreatic involvement, and kidney degenerations aid in produc- 
ing the ultimately fatal result. 

The symptoms may so closely resemble those of acute yellow 
atrophy of the liver as to make a differential diagnosis impossible, 
unless some evidence of the presence of phosphorus is obtainable. 

Vomiting of a nervous type is a common complication of exoph- 
thalmic goitre, and when it occurs sometimes develops into a danger- 
ously severe symptom, owing to its constancy, violence, and resist- 
ance to treatment. Oftentimes serous diarrhea is associated with it, 
and these two associated symptoms should not mislead the physician 
into a diagnosis of cholera morbus nor of jaundice, for icterus often 
comes on. 

Meniere's disease is associated with vomiting, the contents of the 
stomach being expelled after the attack of vertigo and tinnitus 
aurium. 

The affections of the liver which sometimes result in vomiting 
are chiefly catarrhal and obstructive jaundice, hepatitis, hepatic 
abscess, and pylephlebitis. The rapid development of jaundice, 
hepatic tenderness, and swelling, or a history of violent hepatic pain 
(colic), renders the diagnosis possible in the case of jaundice. (See 
chapter on the Skin.) Hepatitis — that is, hepatic abscess — is often 
accompanied by or produces vomiting which is apt to be very obsti- 
nate. The swelling of the liver, the tenderness in the hypochondrium 
on palpation, the pain in the hepatic region, often referred to the 
neighborhood of the right shoulder, and the febrile movement, which 
is intermittent, sweeping up to 104° or 105°, then down to normal, 
are the chief characteristic symptoms. (See chapter on the Abdo- 
men.) Vomiting accompanied by a similar train of symptoms also 
occurs in cases suffering from pylephlebitis. 

Violent vomiting associated with great pain in the loin, radiating 
down into the testicle, or inside of the thigh, indicates the presence 
of a renal calculus, either in the pelvis of the kidney or in the ureter. 

Hemoglobinuria is sometimes accompanied by vomiting. The 
attacks are paroxysmal, and are often ushered in by persistent 
yawning, with pain in the limbs, headache, nausea, and vomiting, 
followed by moderate fever, which is preceded or accompanied by 
a chill. Pain may be felt in the liver, but, more pathognomonic 
than all, the urine is soon found to be dark, brownish red, or even 
black, owing to the presence in it of hemoglobin. 

Vomiting is a frequent coincident symptom of headache, because 
in many cases the headache depends for its existence upon a dis- 
ordered stomach or disordered bowels; but it also appears as a 
characteristic symptom of a condition in which the stomach is pri- 
marily not at fault, namely, in migraine or hemicrania, in which, 
in addition to violent pain in the head on one side, we may have 



VOMITING 523 

hemianopsia, scotomata, and sometimes great pallor or flushing of 
the face. (See Pain.) Usually the vomiting follows the pain. 

\\ hen vomiting occurs in yellow fever, the presence of an epidemic, 
the suffusion of the eyes, the headache, the black character of the 
vomit, the slow pulse, scanty urine, and prostration, all point to the 
cause of the symptom. 

Vomiting is a frequent symptom in some cases of phthisis, par- 
ticularly if laryngeal tuberculosis is present. It also occurs as a 
result of swallowing the sputum instead of expectorating it, and 
very commonly excessive cough produces vomiting, especially if the 
cough follows closely after a meal. 

Closely associated with the vomiting due to these causes is that 
occurring in cases of pulmonary gangrene. 

In children suffering from whooping-cough vomiting often takes 
place at the close of the paroxysm, and is due to the spasmodic 
movements of the chest and diaphragm. 

Finally, it is not to be forgotten that vomiting often ushers in any 
one of the eruptive diseases, such as the fevers, syphilis in its early 
secondary stages, and erysipelas. 

ruder the name of niervcismus cases of voluntary regurgitation 
of food have been reported, chiefly outside of the United States. The 
patients have been nervous or hysterical persons. 

The Vomit. — Aside from the diagnostic significance of the act of 
vomiting, the physician should remember that the vomit itself may 
give him information as to the condition of his patient. 

Under the head of gastric dilatation we have spoken of the signifi- 
cance of vomiting large amounts of Liquid and undigested food, so 
that it is not necessary to speak of this point here; but it is well to 
remember that small amounts of vomited material often possess 
considerable diagnostic importance. In the severe retching of 
cerebral disease or uremia very little material is gotten rid of, and 
this may be ammoniacal. In cases in which small quantities of 
exceedingly sour, clear liquid are vomited, we often find that the 
attack is due to migraine or nervous headache. If watery liquid and 
mucus are vomited, there is probably gastric catarrh. The vomiting 
of bile is usually only seen when repeated retching has drawn this 
secretion into the stomach. The liquid may be either golden yellow 
or greenish in hue. Somewhat like this vomit is that seen in peritoni- 
tis, in which disease grass-green material is often expelled. Similar 
material is also vomited in cases of intestinal obstruction before 
stercoraceous vomiting comes on. 

The vomit of intestinal obstruction is sometimes fecal in odor for 
obvious reasons. If odorous poisons have been taken, the vomit 
smells of the poison; and if there be phosphorus present, the vomit 
not onlv smells of it, but in addition may be luminous in the dark. 



524 HICCOUGH, VOMITING, REGURGITATION 

The significance of bloody vomit has already been described. It 
only remains to name the test for hemin, which, if present, shows 
that the color of the ejecta is really due to blood. Some of the 
vomited material is filtered, and a little of the filtrate is evaporated 
on a watch-glass. This dried material is now scraped off the glass, 
mixed with a trace of finely powdered common salt, and placed on 
a glass slide. The powder is now covered by a cover-glass and one 
or two drops of glacial acetic acid allowed to flow under the cover- 
glass. This is then dried by exposing it to gentle heat, and after 
the drying is absolute a drop or two of pure water is touched to the 
edge of the cover-glass. Very minute crystals of hemin are now seen 
with the aid of the microscope. 



CHAPTER XIX. 

COUGH AND EXPECTORATION. 

The varieties of and diagnostic significance of cough — The causes of cough — 
The sputum — Its pathological significance. 

The significance of cough as a symptom is very important, and, 
though it may arise from many causes, in the majority of instances 
it points to disease in the chest, in the trachea or the larynx, in the 
pharynx or in the nose. Rarely it is a purely nervous trick, and 
equally rarely it arises from irritation in the stomach ("stomach 
cough/' so called). A cough is said to he dry and hacking when it 
fails to bring up into the throat or mouth any secretion, or when it 
is short and sharp. Often such a cough is paroxysmal; in other 
cases it consists in single but fairly frequently repeated, short, and 
forcible expiratory efforts, as if the patient was trying to clear his 
throat. A loose cough is nearly always paroxysmal; that is, it occurs 
"in spells," and at nearly every paroxysm results in the raising of 
some mucus. The first variety of cough is that seen in the early 
stages of phthisis pulmonalis, acute bronchitis, or pneumonia, before 
any exudation has taken place; in the early part of a paroxysm of 
asthma; in the early portion of an attack of whooping-cough and 
when the cough arises from irritation in the upper air-passages, 
whether this be due to the inhalation of dust or the presence of some 
growth, as a laryngeal papilloma. The loose variety of cough is 
seen in the later stages of acute bronchitis, pneumonia, asthma, 
whooping-cough, and in cases of emphysema with bronchiectasis, 
and in the stage of pulmonary tuberculosis associated with the break- 
ing down of lung tissue, the formation of cavity, and the development 
of bronchitis with it, and in gangrene of the lung. 

There are two peculiar forms of cough to be mentioned, namely, 
the so-called barking, brassy, laryngeal cough, which we hear most 
typically in false or spasmodic croup, and the cough of whooping- 
cough, which is, as its name implies, the most typical which we meet 
with. Suddenly the child begins to give a series of quick, sharp 
coughs, which become more and more rapid until the chest is emp- 
tied of air. In the early stages of the disease this is all that occurs, 
and unimpeded inspiration ensues; but later the cough no sooner 
ceases from exhaustion of the lungs of air than with the attempt of 
deep inspiration the glottis closes spasmodically, and the air is sucked 



520 COUGH AND EXPECTORATION 

through the chink with a whooping sound. The flushed or cyanotic 
face of the child, associated with these paroxysmal attacks, renders 
the diagnosis easy. 

There is nothing distinctive in the cough of early stages of pul- 
monary inflammation, whether it be bronchial or vesicular, although, 
if the bronchitis be very intense or if the pulmonary inflammation 
also affect the pleura, the cough may be partly smothered or sup- 
pressed by the patient, who endeavors to control or stop it in order to 
escape the pain it causes. To this end he sits or lies in bed, endeavors 
to fix the muscles of his chest so that they will not respond to the 
reflex cough impulse, and shuts his lips to hold his breath in, although 
very often the reflex irritation overcomes his will-power and the 
cough bursts through his compressed lips with an expression of 
pain. Such a cough is always indicative of pain. 

In all forms of dry cough there is now and again a small plug of 
mucus expelled from some part of the respiratory mucous membrane. 
Such coughs possess no value to the patient, being merely a sign of 
reflex irritation; but a loose cough, unless it is very excessive, is of 
the greatest possible use to the patient, for it is an effort on the part 
of nature to rid the lungs of abnormal exudations or secretions. 
For this reason this symptom is not to be removed completely in 
cases of resolving pneumonia, pulmonary tuberculosis, or bronchi- 
ectasis with excessive secretion, since, if drugs are given which stop 
the cough, the lungs are speedily filled with the secretion; and in the 
case of tuberculosis or gangrene or mucopurulent bronchitis septic 
absorption with systemic infection results. Similar good results are 
reached by the cough heard in cases of pulmonary abscess, and when 
an empyema has broken into a bronchial tube. When the patient 
complains of chronic cough, which is worse in, or confined entirely to, 
the morning hours, and tells us that the cough finally causes the dis- 
charge of much secretion, and that this is followed by freedom from 
cough for many hours, the case may be one of tuberculosis with 
cavity, pulmonary abscess, empyema which has ruptured into a 
bronchus, or sacculated bronchiectasis. Such coughs come on in 
paroxysms whenever the lung must be relieved, and the length of 
paroxysm depends upon the looseness of the secretion and its situa- 
tion in the lung. Thus, if the secretion be in the larger bronchial 
tubes, it is easily expelled; whereas if it be in smaller bronchi, or 
in the vesicles, or at the bottom of a cavity, great and frequently 
repeated effort will be required before the liquid can be raised into 
the mouth for expectoration. 

The presence of an obstinate cough due to bronchitis, which 
resists all ordinary treatment, should lead the physician strongly to 
suspect that one of two ailments is present, namely, undiscovered 
tuberculosis, cardiac failure, or Bright's disease. 



COUGH AND EXPECTORATION 527 

Cough brought on by changing the position of the patient often 
krises became of the alteration in position of a pleural effusion. 

The cough of acute laryngitis may be quite severe, and occurs in 
short, sharp barks of a harsh or brassy character (like spasmodic 

eronj)) which is so typical as to l>o called a laryngeal cough. The 
association with this cough of partial or complete loss of voice and 
pain in the larynx, with a history of exposure to cold and dust, or 
of the excessive use of the larynx in speech or singing, renders the 
diagnosis clear, even if the laryngoscope i- not used to discover con- 
gestion and inflammation of the laryngeal mucous membrane. In 
the false croup of children, which is always associated with laryngeal 
irritation, the barking, ringing cough i- so characteristic a- to render 
a diagnosis possible as soon as the sound is heard, and with it there 
is dyspnea due to obstruction to breathing. 

The cough of the Laryngeal phthisis is not so typically brassy and 
ringing as that of acute laryngitis, but the presence of pain in the 
larynx, hoarseness, and persistent laryngeal dryness and difficulty 
should lead to a search for tuberculosis by the laryngoscope, and an 
examination of the chest for physical signs of trouble in the lungs 
and of sputum for tubercle bacilli. 

Sometimes cough of a laryngeal character is due to an aneurysm 
pressing upon the larynx. In other cases the cough depends not 
upon the pressure of an aneurysm, but upon the pressure produced 
by carcinoma of the esophagus, by a mediastinal tumor. 

Cough due to the inhalation of irritant dusts or vapors is often 
present in girls who work in carpet factories, in the air of which 
there are immense quantities of fine particles of wool. Again, it is 
seen in knife grinders, needle workers, coal miners, and in workers 
in arsenical and lead pigments. 

Sometimes in paralysis of the pharyngeal muscles glossolabio- 
pharyngeal paralysis) cough is produced by the slow passage of 
food, which may in fact enter the larynx. 

A night or evening' cough is very commonly seen in cases ^^' respira- 
tory catarrh or more grave disease. It is often absent all day, only 
to return in the evening in cases of laryngitis and in phthisis; and 
in those cases in which it follows getting into bed, it is due to chilling 
of the skin by the cold sheets, which results in congestion of the 
inflamed mucous membrane. 

Quite frequently children suffering from chronically enlarged 
tonsils suffer from cough on going to sleep, especially if the uvula is 
relaxed or elongated. The cause of this cough is that in the relaxa- 
tion of sleep the tonsils touch one another or tickle the uvula. As 
soon as "the child wakes muscular contraction separates the approxi- 
mating surfaces and the cough soon ceases. 

If this cause of cough cannot be eliminated we must look farther 



528 COUGH AND EXPECTORATION 

for its origin. Not infrequently hypertrophy of the mucous mem- 
brane over the turbinated bones, so that it presses on the nasal 
septum, may cause cough, and irritation of the inferior and middle 
turbinated bodies and the septum opposite the inferior turbinated 
body may cause reflex cough. So, too, enlargement of the pharyn- 
geal tonsil may cause this symptom, as may also elongation of the 
uvula. When chronic enlargement of the tonsils, with follicular 
accumulations, is present, cough frequently results. 

In regard to coughs in general, it can be said that in the absence 
of the early stages of acute inflammation of the respiratory apparatus 
a dry, hacking cough is either nervous or is due to reflex irritation 
in the ear or stomach, or to some hyperesthetic spot in the nasal, 
pharyngeal, or laryngeal mucous membrane; whereas a loose cough 
may arise both in adults and children from congestion and engorge- 
ment of the lingual tonsil. Such a cough is frequent, dry, and 
paroxysmal, and seems to arise from a sticking or pricking sensation 
in the throat; whereas a loose and prolonged cough depends upon 
causes of greater gravity farther down in the respiratory organs. 
Generally, if the stomach is at fault, a low grade of pharyngitis will 
be found. 

The cessation of cough in advanced phthisis, suffocative bron- 
chitis, or the bronchorrhea with bronchiectasis of old persons, or in 
severe pneumonia, indicates exhaustion, collapse, or approaching 
unconsciousness, and is a bad sign. 



THE SPUTUM. 

Macroscopic Examination — A careful examination of the mate- 
rials expectorated by the patient, or, in other words, of the sputum, is 
of the utmost importance in all cases of disease of the respiratory 
tract, whether the abnormal process be primary or secondary. The 
methods which we resort to in examining sputum are macroscopic, or 
those of the naked eye, and microscopic. Of these, the microscopic 
are by far the most important. Sputum varies greatly in its general 
character on ordinary examination, sometimes being very fluid and 
even watery in consistency, and sometimes thick or tenacious. In 
some instances it is clear and glairy-looking, resembling somewhat 
partly beaten white of egg; in others it is yellow and opaque. Placed 
on a clean linen cloth, the sputum may evaporate to almost nothing, 
or leave a heavy mucopurulent deposit after all moisture is gone. 

The naked-eye appearances of sputum are, however, quite char- 
acteristic in several conditions. Thus, in the later stages of acute 
bronchitis the sputum is apt to be thick and yellowish, and to contain 
lumps of half-inspissated mucus. In croupous pneumonia it is 






the sputum 529 



fusty in color, is peculiarly free from watery ingredients, and is 
gelatinous to such an extent that it adheres to the spit-cup, so that 
when this vessel is well filled its contents do not readily fall out even 
when the cup is tipped upside down. The sputum may be less 
adhesive after resolution is well advanced. The brightness of the 
blood in the sputum in cases of pneumonia is also a guide to 
prognosis. Thus, Sir William Jenner said: "The less the weight for 
a given height, the more red blood in the sputum, the better the 
chance for the patient." In pulmonary hemorrhage or hemop- 
tysis, after having, perhaps for a short time, a salty taste 
in the mouth, the patient suddenly brings up, with or without 
much preceding cough, a gush of uearly pure blood or blood freely 
mixed with ordinary sputum. The blood is bright red, not dark or 
prune juice in appearance, and the liquid is frothy, while the cough, 
which is always present after the hemorrhage has occurred, is sup- 
pressed and resisted by the patient, who fears further bleeding. 
This hemoptysis may be caused, first, by pulmonary tuberculosis; 
second, by valvular cardiac disease, generally involving the mitral 
valves, and resulting in pulmonary infarction; third, by aortic 
aneurysm; fourth, in persons suffering from severe purpura; fifth, 
from persons suffering from hemophilia; sixth, from vicarious men- 
struation; and, seventh, in rare cases of hemorrhagic smallpox. 

Bloody sputum must be separated from bloody vomit due to gas- 
tric hemorrhage arising from ulcer or cancer. (See Vomiting.) This 
can be done by the cough, by the frothy character of the expectora- 
tion, by the presence of physical signs in the lungs, and by the history 
of pulmonary disease. It may, however, be confused with slight 
hemorrhage from a dilated and ruptured vessel on the posterior 
pharyngeal wall, in which case, after a little coughing, there may be 
expelled on a handkerchief a little blood-tinged saliva. Examination 
of the throat will usually reveal the ruptured vessel or other vessels 
dilated, but still intact. For a number of days after an attack of 
.hemoptysis there may be expelled in the sputum dark clots of blood. 
So-called "currant-jelly" clots are expelled by coughing in many 
cases of malignant growths of the lungs. 

Other causes of blood-streaked sputum are aortic aneurysm with 
leakage by oozing into a bronchus or the trachea; and particularly 
in children do we see streaks of blood in the sputum if there be present 
pulmonary gangrene. 

Care should always be taken to discover whether the materials 
spit up are really tinged with blood, for they may be colored by some 
dyestuffs or the blood of some animal for the purposes of deception. 
Finally, it is well to remember that a reddish-brown or brick-dust 
looking sputum is sometimes coughed up in cases of hepatic abscess 
communicating with the lung; and the sudden expectoration of a 
34 



530 COUGH AND EXPECTORATION 

brownish, purulent-looking sputum by a person who has been a 
sufferer from dysentery should cause the physician to examine the 
sputum for the ameba coli, in order to discover if the case is one 
of pulmonary abscess secondary to amebic dysentery. Symptoms 
of hepatic abscess may also be present. This has been called 
"anchovy-sauce" sputum. 

In addition to the sputum already described we sometimes see a 
peculiar semiliquid sputum in cases of pulmonary phthisis, in which 
the sputum promptly separates into two layers on standing, the 
upper one being light and flocculent, unless there is a well-marked 
bronchial catarrh present, when it may be markedly mucopurulent, 
or, if a large cavity is present, its purulent character may be even 
more marked. To this list may be added several others, namely, 
the purulent sputum of pulmonary abscess or empyema, of medias- 
tinal abscess opening into a bronchus, subphrenic abscess, hepatic 
abscess, pronounced bronchiectasis, and that from a large tuber- 
culous cavity in the lung. Of these the more common are bron- 
chiectasis, tuberculous cavity, and empyema breaking into a bron- 
chus. In the first of these the cough is paroxysmal, and after it 
has been kept up for some time a gush of purulent sputum is 
suddenly brought up into the mouth, and the accumulation of pus 
is removed for a time. In the other the sputum is very fluid, and 
is so free that its expectoration rapidly fills the spit-cup, provided 
that the patient is strong enough to bring it up. A very liquid 
watery sputum is seen in pulmonary edema, particularly that seen 
in cases of Bright's disease or heart failure, and in some of the 
pulmonary forms of epidemic influenza. 

Sputum which, on standing, separates into three layers, the top 
one frothy and dirty looking, the next clear and filled with shreds, 
and the lowest consisting of a sediment of pus and broken-down- 
looking materials, is seen in cases of pulmonary gangrene, and if 
the sputum when placed in a vessel containing water sinks to the 
bottom in disk-like masses or globules the disease may be tuberculosis. 

The sputum expelled by an asthmatic at the time of the attack 
also has characteristics not so easily seen at a glance, but nevertheless 
demonstrable by the naked eye. Small pearls or plugs of mucus of 
the size of a sago-pearl are seen in the sputum, and if these are 
placed on a plate of glass under which is a black surface, and then 
teased out, they will be found to be rolled-up fibers, which when 
unrolled are found to be in the forms of curls or spirals. These are 
sometimes called Curschmann's spirals (Fig. 197), and they are 
rarely seen in several other conditions than asthma, namely, in 
chronic pulmonary tuberculosis and croupous pneumonia. Through 
the central core of the curl runs a bright and refractive filament, 
which is waxy, and is probably not an entity, but an optical effect. 



THE SPUTUM 531 

Between the spiral fibers can be seen in many cases slight, bluish, 
octahedral crystals varying greatly in size, sometimes requiring a 
high-power lens to distinguish them. They are said by Salkowski 
to be composed of a mucous substance, but others believe them to 
be oxalate of lime, a phosphate of an unknown base, or ethyjenimin. 
These are called Charcot-Leyden crystals, and are also seen in the 
sputum of chronic croupous pneumonia, chronic pulmonary tuber- 
culosis, and in acute bronchitis. 

Sometimes, in cases of diphtheria, casts of the larynx and upper 
bronchial tubes are expelled by coughing. Small casts are also seeu 
in the sputum of that rare affection, fibrinous bronchitis. Some- 




Fig. 197. — Curschmann's spirals. (Von Noorden.) 

times these casts consist of a perfect mould of several branching 
bronchial tubes and bronchioles, and they may be white, yellowish, 
or even pinkish in color from bloody exudation. Sometimes they 
are only visible to the naked eye if placed in water and shaken, 
when what has appeared to be a roll of mucus spreads out into the 
characteristic shape of the tubes from which it comes. Casts of 
the finer tubes can sometimes be found in the sputum of cases of 
croupous pneumonia. 

Microscopic Examination. — The examination of the sputum by 
the aid of the microscope should be made with care. A portion of 
the sedimentary part of any sample may be carefully separated from 



532- COUGH AND EXPECTORATION 

the rest by means of a pipette ; but to facilitate the examination of 
sputum for tubercle bacilli when but few exist, for the rapid and 
thorough examination of the sputum for elastic fibers, which has 
been heretofore a tedious and complicated process, and for the dis- 
covery of Charcot-Leyden crystals and fibrinous coagula, the centri- 
fuge is a much better apparatus.. (See chapters on Urine and Blood.) 
The tubes used for the precipitation of the sputum are 50 mm. long, 
with 2\ mm. lumen, and are fitted into the hematocrit frame. 

A small quantity of sputum is placed in a clean porcelain dish 
and actively stirred for a few minutes with a glass rod until it becomes 
thin and free from lumps and apparently homogeneous. Without 
any dilution whatever the sputum is drawn into the sputum tubes 
by means of a medicine dropper connected with a small rubber tube. 
The two precipitating tubes, filled with sputum in this way, are 
placed in the hematocrit frame and revolved for at least three 
minutes, making about 15,000 revolutions. The solid portions of 
the sputum collect in the distal extremity of the tubes. A small 
portion of the sediment is placed on a slide and examined micro- 
scopically for elastic fibers, Charcot-Leyden crystals, etc. The sedi- 
ment from the second tube can be stained for tubercle bacilli or other 
microorganisms as desired. 

When the centrifuge is not used and a small particle of sputum 
is placed upon a glass slide under a cover-glass and gently pressed, 
there will be seen, if the sputum be mucous or mucopurulent, threads 
of mucus and mucous corpuscles with white blood corpuscles, which 
are particularly numerous if the sputum be purulent. These latter 
are granular, fatty, and sometimes pigmented by soot or other sub- 
stances which have been inhaled. Epithelial cells derived from the 
respiratory passages are also found in large numbers, often broken 
down and fissured, granular, and generally a nucleus can be distin- 
guished in their centre. Of far more importance than these, how- 
ever, are the particles of elastic fiber or elastic threads, which, if 
present, show positively .that a breaking-down process is going on 
in the lung, or more rarely in the bronchial tubes. These are usually 
seen in the sputum of advanced or rapidly progressing tuberculosis 
of the lung and in that of abscess and gangrene of the lung. If 
there is doubt as to their presence because they are sparse, we obtain 
them by the following process : boil equal parts of the suspected 
sputum and a 10 per cent, solution of caustic potash, and dilute the 
jelly-like mass which results with water. After this has stood for 
twenty-four hours the elastic fibers may be found in the sediment as 
swollen threads, for which, however, small particles of food which 
may come from the mouth may be mistaken. 

The appearance of fine, needle-like crystals of fatty (margaric) 
acid, which may be bent like a curved needle and often grouped in 



THE SPUTUM 



533 



bunches, may indicate pulmonary gangrene or purulent bronchitis. 
They are found chiefly in the plugs or lumps which the patient 
expels in his sputum, but they possess no indicativeness of the 
pulmonary changes just named if follicular tonsillitis, either acute 
or chronic, is present, since the plugs derived from the follicles of 
the tonsils also contain similar crystals. Again, they are of no diag- 
nostic value it* found in stale, mucopurulent sputum, as they may 
form in this after it has been expectorated. The peculiar crystals 
called Charcot-Leyden crystals have already been described. 

There are four remaining objects to be seen in the sputum of dis- 
eased persons, all of which are of great diagnostic importance when 
found. The first of these is very rare, namely, the eggs of the Distoma 
pulmonwn, which are found in the sputum. This parasite some- 
times produces hemoptysis without any physical signs of pulmonary 
change, is rarely if ever seen in this country, but is common in 
o 





Fig. 198. — Actiiiomvee<. 



Japan, Corea, Formosa, and China. The second is the evidence of 
eehinococcus infection by the appearance of portions of the cysts or 
of the hooks of the scolices when the cyst bursts into a bronchus 
from the lung or adjacent structures. Such cases are also rare in this 
country. The third condition, which is also very rare when involving 
the lung, is actinomycosis, in which infection we find radiated fungi 
or actinomyces in the sputum. This fungus appears as a number 
of club-shaped projections attached to a heterogeneous mass of 
irregular-looking material (Fig. 198). 

The fourth and most important of all these finds in sputum is the 
tubercle bacillus, both from the point of diagnosis, prognosis, and 
treatment, and because the disease tuberculosis is so widely distrib- 
uted in every class, in every part of the country, and is so constantly 
prevalent. The discovery of this bacillus in a sample of sputum 
which has not been exposed to the entrance of bacilli after it has been 
expectorated, is a positive sign of tuberculous infection of the lung 



534 COUGH AND EXPECTORATION 

unless there be tuberculous disease of the upper air passages or 
mouth. While their presence gives positive evidence, their absence in 
a given sample of sputum is not negative evidence of an absolute 
character, for that particular specimen may be free from bacilli or 
they may have escaped the staining or the eye of the examiner. 

The method for examining sputum for tubercle bacilli is' as follows : 
The specimen which is brought to the physician is poured into a shal- 
low glass vessel having a blackened bottom, or into a glass saucer 
placed on a piece of blackened paper. If this sputum is now closely 
examined, it will be found to contain small, yellowish masses, one 
of which should be picked up by means of a spoon or platinum 
needle, freeing it as much as possible from the mucus surrounding it. 
A very small part of this mass is now placed on a cover-glass and well 
distributed over its surface by means of a needle or teasers, or it is 

'} ' v " Ni \\ . A 







Fig. 199. — Tuberculous sputum stained by Gabbett's method. Tubercle bacilli seen as red 
rods ; all else is stained blue. (Abbott.) 

spread by placing another cover-glass over the first and pressing 
them together with a to-and-fro movement. The quantity of sputum 
used must not be large enough to extend over the edges of the glass. 
This having been done, the glasses are now separated by a gliding 
movement, and the thin film of sputum covering each one is allowed 
to dry by exposure to the air, after which, being held by forceps, it is 
passed through the flame of an alcohol lamp to fix the coating. Care 
must be taken that too much heat is not used. Some carbol-fuchsin 
stain 1 is now placed in a watch-glass and the cover-glasses are 
immersed in it. As soon as this is done the cover-glass is held over a 
flame until the steam begins to rise from it, when it is withdrawn, 
then heated again until this process has been repeated several times. 
The cover-glass is now washed in water, and the film covering it will 
be found to have an evenly distributed red color. The glass is next 

i Carbol-fuchsin stain, or Ziehl's solution, is made by dissolving 1 gram of fuchsin in 
10 c.c. of alcohol, and adding 100 c.c of a 5 per cent, solution of carbolic acid. 



THE SPUTUM 535 

placed for a moment in a 2.5 per cent, solution of nitric or sulphuric 
acid in water and gently moved about, to decolorize the deposit on the 
surface of the glass. As a result the albumin and cells on the glass 
are decolorized, but the bacilli are not. The glass is next washed in 
dilute alcohol (bO per cent.) to remove any free fuchsin. Should the 
decolorization be imperfect, so that the film still has a red color, it 
must be still further decolorized by returning the glass to the acid 
solution and then washed again in the dilute alcohol and water. The 
cover-glass is now placed in a solution of methylene blue (saturated 
watery solution). The glass is then finally washed in water, and 
afterward examined under the microscope, or dried and mounted in 
Canada balsam for permanent preservation. The tubercle bacilli 
are distinguished by the fact that they retain the red color from the 
fuchsin solution, while other bacteria, having been decolorized by 
the acid solution, take the contrast stain and appear blue. 

Another method, Gabbett's, is perhaps more useful than that jusl 
given. It consists in staining, as already directed, with the carbol- 
fuchsin solution, and then placing the cover-glass in a second 
solution, which contains the acid for decolorizing and the contrast 
stain. This latter solution is composed of 100 c.c. of a 2.") per cent. 
mixture of sulphuric acid and methylene blue 1 to 2 gin. The 
cover-glasses are left in this solution for a couple of minutes, and 
then washed in water. When placed under the microscope the 
tubercle bacilli will appear as red rods in strong contrast to the 
blue background. 



CHAPTEE XX. 

PAIN. 1 
The kinds of pain — The significance of its locality — Colic. 

It is manifest that it will be impossible for the author in this 
chapter to enumerate all kinds of pain, both as to the situation, 
degree, and character. He can only mention those forms which 
possess considerable diagnostic importance. It should always be 
remembered that pain is the sign adopted by Nature to notify the 
individual of some abnormal condition in his body, and in many 
instances pain is only developed when the attempt is made to move 
a part which from its condition had much better be allowed to rest. 

Pain is generally described as darting or stabbing in character, 
when it occurs in a single or repeated paroxysm; as throbbing or 
pulsating, when it rises and falls in severity with the pulse beat; as 
dull and aching, when it resembles the feeling associated with a 
bruise. Sometimes stabbing or darting pains are called lancinating, 
or the patient may state that the pain is tearing and rending in 
character. All pain is associated with direct or indirect irritation 
of nervous matter, but, if the nerve or nervous centres connected 
with a part be destroyed organically or arrested in function, we have 
a condition called anesthesia. (See chapter on the Skin.) 

Not infrequently darting or stabbing pain is associated closely 
with actual disease of nervous tissue, which may be primary or 
caused by the pressure or irritation of a growth or some foreign 
body. Such pains are seen in neuralgias due to inflammation of the 
sheath of a nerve or its surroundings as it passes through a bony 
foramen; in neuralgia due to meningeal thickening; in the lightning 
or tearing pains of locomotor ataxia; from pressure upon the spinal 
nerves by spinal disease or in that caused by fractured bones. Again, 
we often meet with violent pain as the result of true neuritis, whether 
it be produced by infection, by injury, or by poisoning. 

Throbbing pain is nearly always associated with the presence of 
congestion or local swelling in the part where the pain originates, 
and arises from the fact that the peripheral nerves are subjected to 
pressure, which is increased with each additional beat of the heart. 
Dull, aching pain is often produced by slow inflammatory or patho- 
logical processes in organs not well endowed with sensory nerves. 

» See also chapter on Headache. 



PAIN 537 

There are two forms of pain yet to be considered which are pecu- 
liar in their character, namely, that nauseating pain due to a blow 
or injury to the testicle and ovary and that boring pain which occurs 
in cases of inflammation or morbid growth affecting bony tissues, 
particularly in the long bones. 

There is another point in connection with the study of pain as ;i 
symptom of disease, namely, that pain is often referred to a point 
far away from the source of the symptom. Thus, the child with 
hip disease complains of pain in the knee or in the ankle; the one 
with dorsal caries, of pain in the intercostal nerves anteriorly; and 
a stone in the kidney may cause violent pain in the penis or testicle. 

The physician should always remember that the degree of pain 
must be determined in part by the expression of the face and move- 
ments of the body, for often these features of a case will show that 
the pain described so vividly in words is much exaggerated. The 
general systemic signs of pain are a tense pulse, if the pain 1 e recent 
in onset and acute; a somewhat accelerated respiration unless the 
pleurae or lungs are involved, when it may be retarded; dilatation 
of the pupil; more or less sweating, particularly on the forehead; 
faintness; and sometimes the passage of clear, limpid urine if the 
pain be abdominal. 

The first kind of pain which will be discussed is the darting or 
paroxysmal pain in what may be called the neuralgias. These 
depend upon one of three causes, and, though they may occur in any 
nerve of the body, are most commonly seen in the nerves of the head ; 
or in nervous women in the nerves of the pelvic organs and external 
genitals. The three causes are generally debility with anemia, reflex 
irritation, and irritation of the nerve by poisons or by the presence of 
growths. 

Violent neuralgia of the head is commonly seen in overworked 
or overdanced young women, who lack sufficient sleep and fresh air 
and who are anemic. It also arises from the reflex irritation of a 
decayed tooth, or from inflamed or overstrained eyes, or from a dis- 
eased ear, so that an examination of any one of these parts may 
reveal the cause of an obstinate neuralgic pain. Similarly we see 
cases of neuralgia, particularly of the supra-orbital nerve, which are 
due to chronic poisoning by one of the metallic poisons, such as lead 
and arsenic, and also as a result of malarial infection (brow ague). 
If the neuralgic pain be due to neuritis, it will not only be typical 
of neuralgia, but along the track of the nerve marked tenderness 
will be developed on pressure, and rarely an eruption will appear on 
the skin, as a herpes zoster. Pure neuralgia, on the other hand, is 
often relieved by pressure upon the nerve involved. 

When the fifth cranial nerve is affected by neuralgia, we find that 
if the upper branch is involved the pain is felt in the forehead, the 



538 



PAIN 



eyebrow, and the eyeball, the conjunctiva often becoming injected 
If the pain be in the upper lip, the posterior nares, and the cheek, 
the infra -orbital or second branch is affected; while if the pain is in 
the lower jaw and chin, the third division of the fifth nerve is involved. 
A peculiar form of neuralgic pain coming on in attacks or par- 
oxysms of great severity is migraine or megrim, in which the pain is 
usually confined to one side of the head, associated with great tender- 
ness of the scalp, and may be preceded in many cases by disorders 
of vision, such as hemianopsia or dimness of visual perception. 
Associated with this pain at its zenith we frequently see vomiting 
and retching, faintness, with sweating localized in the pain area, or 
diffused, and great facial pallor. Pressure by the fingers upon the 




Figs. 200 and 201.— Showing the distribution of the three branches of the fifth nerve. 



painful area often produces no more pain or even gives partial relief, 
but a light touch may cause increase in the pain. Rarely a somewhat 
similar condition to migraine, which is not unilateral but bilateral, is 
found in connection with rheumatism of the scalp. As migraine may 
be due to a rheumatic state, care in making a differential diagnosis 
is necessary. The pain of migraine is, however, unilateral, more 
severe, more transitory, and associated with the symptoms named, 
whereas in the rheumatic head pain the history of rheumatic ten- 
dencies of a marked character, the diffuse pain, the increased soreness 
on exposure to cold or changes in the weather, aid in separating it 
from migraine. 

When syphilis or injury causes a 'periostitis of the skull, violent 






PAIS 539 

pain of a neuralgic character may be present, particularly at night; 
but the local symptoms arc manifest, and when compared with the 
history make the diagnosis possible. 

It is also necessary to separate the headache of cerebral tumor or 
cerebral abscess from neuralgia of the head. The pain of such a 
cerebral condition is constant; the headache is sometimes worse ;it 
night, sometimes in the daytime, and greatly increased by physical 
or mental effort. The danger of confusing the pain of neuralgia 
with that due to tumor is great unless the physician remembers that 
the constant pain of tumor may vary from slight headache to sharp 
paroxysms of pain. The occurrence of convulsions points strongly 
to tumor if associated with headache of this character, and, finally. 
the presence of tumor as a cause of headache and not ordinary neu- 
ralgia is decided by evidences of optic neuritis, vomiting, vertigo, 
and the development of focal symptoms of localized paralysis. 
(See chapters on Headache, Vomiting, Convulsions, and Spasms. 

The most common seat for neuralgic pain in the head, other than 
in the brow, is the occipital region, the posterior branch of the second 
cervical nerve or great occipital being the one most affected Fig. 
201). As this nerve supplies the occipital region and the posterior 
part of the parietal regions, the.se areas may be involved in the painful 
manifestations, and all these parts may be tender to the touch. 
Brushing the hair may be impossible, because of the pain produced 
by the brush touching the seal]). Occipital neuralgia is oftentimes 
bilateral. It may simply arise from cold or injury; but, if persist- 
ent and severe, caries of the cervical vertebra should be sought for 
as a possible cause. 

Pain of a neuralgic or darting character in the neighborhood of 
the heart is found as the result of several causes, as a rule in the 
following order of frequency: (1) Pain with palpitation of the heart 
from the accumulation of flatus in the transverse colon just as it 
turns to descend. Many patients who come to the physician com- 
plaining of heart disease suffer only from this condition, due to 
fermentation in the large bowel. Again, the pain due to gastralgia, 
or, as it has been called, cardialgia, may be referred to the heart by 
the patient. (2) To intercostal neuralgia due to debility. In these 
cases a tender spot will often be found, one in the precordium, 
another in the outer edge of the scapula, and a third on the vertebral 
column. These are sometimes called the "spots of Valleix." In 
other cases the pain will be due to spinal disease, anemia, or the 
tight lacing of corsets. (3) To pseudo-angina. (4) To true angina 
pectoris. (5) To locomotor ataxia. 

Pain of a character somewhat resembling true angina pectoris is 
also sometimes met with in patients who have that rare disease, 
acute aortitis. The pain is constant under the sternum, but it lias 



540 PAIN 

terrible exacerbations, and a sensation of rending of the retrosternal 
tissues. Death may occur in an attack. It is seen chiefly in gouty 
patients and in syphilitics. Very rarely it is seen in patients who 
have suffered from malarial poisoning. 

Pain is felt much more commonly in disease of the aortic orifice 
than in lesions of the mitral orifice of the heart. 

Pseudo-angina occurs most commonly in anemic, nervous girls, 
or young women whose vessels are normal but who have hysterical 
tendencies. True angina occurs in those of middle age or advanced 
life or in young persons whose vessels are affected by syphilis. In 
the false form the sensation is as if the heart would burst. In the 
real form it feels as if the heart were squeezed tightly in a vise. In 
this form, too, the bloodvessels will usually be found hard and corded, 
atheromatous, and the blood pressure high. The additional diag- 
nostic points in favor of true angina pectoris are that the principal 
seat of pain is somewhat to the left of the lower and middle sternum, 
from which spot it may extend to the axilla and back and turn off to 
the occiput or extend down the arms to the hands, where a sensation 
of coldness may be felt. Sometimes even the abdominal organs and 
testicles seem to be affected. The patient is motionless, the. face 
anxious and covered with a cold sweat, and respiration is shallow. 
The disease is usually seen in persons over forty years of age. The 
thoracic pain of locomotor ataxia is rarely felt in the precordium, 
but commonly in the axilla, and it rarely radiates down the arm. 
The other symptoms of tabes dorsalis should be sought for in all 
doubtful cases. (See chapter on the Legs and Feet.) True angina 
pectoris is far more rare in women than in men. Violent cardiac pain, 
exactly resembling that of true angina pectoris, is met with, according 
to Vergely, in diabetes mellitus. 

Very severe pain, paroxysmal or constant, felt in the chest may 
also be due to aortic aneurysm, and, if so, will be found associated 
with pain shooting down the arm on the left side, dilatation of the 
pupil, unilateral sweating of the face and neck, and the physical 
signs described in the chapter on the Thorax. 

Severe pain of a darting character felt in the chest, not due to 
angina or. the causes just named, is nearly always an indication of 
one of four things: (1) Intercostal neuralgia, already named; (2) 
pleuritis, with or without pneumonia; (3) pericarditis, if it is felt in 
the precordium; (4) a morbid growth in the chest, particularly a 
mediastinal tumor or enlarged bronchial glands. 

Both intercostal neuralgia and pleurisy are associated with severe 
pain, increased by taking a deep breath, the pain occurring some- 
times with inspiration and sometimes with expiration. They are to 
be separated from one another by the presence of cough, fever, and 
of a friction sound in pleuritis, and by the fact that the entire side 



PAIN 541 

is more or less tender to the touch in this state. When the pain is 
constant and lasts for a long time, it may be due to a low-grade 
pleuritis, resulting from pulmonary tuberculosis, particularly of the 
apex of the lung, the morbid process affecting the pleura. Pericar- 
ditis is frequently caused by pneumonia, arid is painful. 

Pain felt at the right of the left scapula or between the shoulders 
is often due to gastric ulcer or dyspepsia. 

The pain of mediastinal growth is due to pressure on nerve trunks, 
and the diagnosis may be very difficult unless bulging and dulness on 
percussion are present. The condition is rare. 

Neuralgia of the pelvic viscera in women is frequently seen as the 
result of functional or organic disease. It may be ovarian, when it 
is very apt to occur with greatest severity half-way between the 
menstrual epochs or just before them. Sometimes the neuralgia 
may be present in the labia majora or in the perineum. It usually 
occurs simply as a sudden, darting pain, which does not last, and, 
indeed, rarely continues more than a moment, although there is 
usually associated with it more or less constant uterine or ovarian 
tenderness. Care should be taken that these pains are not thought 
to be due to cancer or other severe organic lesion. Pain in the sacral 
region is often an indication of uterine or rectal disease. If higher 
up the back, it is often due to myalgia or lumbago; and lumbago, 
if not due to rheumatic tendencies, is often due to the colon being 
loaded with feces. 

If the patient is a child, pain in the back should cause us to suspect 
spinal caries, rickets, or scurvy. If the former, any jar will greatly 
increase the pain; but if the child be placed over the knees, face 
downward, and the knees separated so that intervertebral pressure 
is removed, the pain disappears. Such a child if told to jump down 
from a stool will not obey, but will take care to slide off gradually 
and gently on to the floor, in order to avoid jarring the spine. 

In scurvy the tenderness of the spine is usually diffuse, but it may 
mislead the physicians into a diagnosis of spinal disease, but inves- 
tigation of the gums will reveal scorbutic blisters and the diet will be 
found imperfect. (See chapter on the Lower Extremities.) 

When a patient suffers from violent pain, increased by motion, 
extending from the sciatic notch in the buttock down the posterior 
part of the thigh, even to the ankle or heel, the pain signifies an 
attack of sciatic neuralgia in an adult, or if it occurs in a child gives 
grave reason for suspecting hip disease. If it is not sciatic neural- 
gia, it is due to sciatic neuritis, or, rarely, to a growth in the pelvis 
pressing upon the nerve before it emerges from the pelvis. The 
pain is fairly constant, generally worse at night, and becomes 
agonizing at times, even if the patient remains absolutely quiet and 
does not move the limb. The following points will, when pressed on, 



542 PAIN 

increase the pain if it be neuritis : the point of exit of the nerve from 
the pelvis, on the lower part of the sacrum, the head of the fibula, 
and behind the malleolus on the outside of the ankle. If these 
points are found, combined with a history of exposure to cold, injury 
to the nerve, rheumatic tendencies, and a persistency and tendency 
to return, the diagnosis of sciatica is clear. If the pain be due to 
sciatic neuritis there may be found wasting in the muscles supplied 
by the nerve, and some anesthesia of the skin, and herpetic erup- 
tions may appear on the skin along the course of the nerves. There 
will be also a history of long duration, and the leg will be apt to 
feel numb and tense from effusion into the sheath of the nerve. (See 
chapters on the Skin and on the Feet and Legs.) The heel and toes 
will be tender, but the inner aspect of the plantar surface will usually 
escape. Again, in sciatic neuritis, if the leg be extended, and then 
while in extension flexed at the hip until it is at a right angle with the 
trunk, pain will be felt at the sciatic notch. When the pain is a pure 
neuralgia, which is rare, it is not increased by moving the limb, there 
is little or no tenderness on pressure on the nerve trunk, and the 
patient often suffers from neuralgia of other nerves. 

Sciatica is much more common in men than in women, which is 
the reverse of all other nerve pains of like character, and far more 
usual in middle or advanced age than in the young. 

Double sciatic pain should arouse suspicion of locomotor ataxia, 
of malignant growth pressing on the spinal cord or on both nerves 
in the pelvis, the presence of lumbar abscess or of diabetes mellitus 
causing neuritis. 

When there is a hysterical, painful joint at the knee or hip in a 
woman, care is necessary to discover that the pain is over the entire 
leg rather than in the course of the nerve. Care must also be taken 
that rheumatism of the muscles of the thigh be not taken for sciatica. 
This can be separated from sciatica by the diffuse character of the 
pain and tenderness and by the fact that in the rheumatic condition 
the slightest muscular movement causes pain all over the thigh. 
Sometimes a malignant growth of the femur may produce symptoms 
of sciatica, and the writer not long since had under his care a case of 
osteosarcoma of the femur which had been treated for sciatica for 
several months. 

Finally, renal calculus may cause violent pain to be felt down the 
leg. (See below.) 

It should also be remembered that malingerers, particularly 
soldiers desiring to shirk duty, often pretend to have sciatica. 

Abdominal Pain. — Abdominal pain of sufficient severity to cause 
a patient to seek medical aid may be due to a large number of causes. 
Its locality is of some value in helping to determine its cause, but 
too much reliance should not be placed upon the statements of the 



ABDOMINAL PAIN 543 

patient as to its site, because even the most intelligent may be unable 
to correctly indicate its actual point of origin. In a general way it 
may be stated that a pain which is most severe in the upper right 
quadrant of the abdominal area is probably due to gallstone colic, 
to cholecystitis, or to disease in the pyloric portion of the stomach. 
So. too, pain in the right lower quadrant is probably due to appendi- 
citis or it may be due to carcinoma of the caput coli, and in women, 
to disease of the ovary or Fallopian tube. Pain in the upper 
left quadrant is most commonly due to wind at the angle of the 
transverse colon and rarely to gastric ulcer, while pain in the left 
lower quadrant is due to gas, to a growth in the bowel or to a sig- 
moiditis or to ovarian or tubal disease. By far the most frequent 
form of abdominal pain is that due to flatus arising from indigestion. 
A peculiarity of this form of pain is the fact that it i-> rarely limited 
to one spot for any length of time, and is usually relieved by the 
passing of gas from the rectum. It may be associated with diarrhea 
and a history of the ingestion of indigestible food. Further than this, 
percussion will elicit a tympanitic note in the area of greatest pain and 
distention, whereas, in intestinal obstruction due to tumor or intus- 
susception, percussion may reveal dulness. (For the various forms 
of intestinal obstruction, see the chapter on Vomiting 

In hepatic colic the patient often, after some days of wretchedness 
and "biliousness," is seized by sudden and violent pain in the right 
hypochondrium, which is paroxysmal in character. Jaundice' ensues 
in such cases with more or less rapidity, and fever of an irregular 
type may occur in the renal form of colic. It is worthy of note that a 
gallstone when in the gall-bladder, or cystic duct, rarely causes much 
pain, and its impaction in this duct does not cause jaundice. If it be 
in the hepatic duct jaundice is present, and pain is often marked. 
but is not so severe as if it be in the common duct. 

If the stone be impacted in the common duct, then the mosl 
violent pain is present, and jaundice is marked, as a rule, the stools 
being clay colored. If the symptoms develop suddenly, and pass 
away equally rapidly, the stone has probably escaped into the bowel, 
whereas if the stone becomes impacted in the papilla? of the duct, the 
jaundice and other symptoms become progressively worse. It is 
entirely possible for the same stone to slip back, and cause tempo- 
rary relief, then to slip into place and precipitate another attack, or 
for another calculus to follow its predecessor, causing a return of 
the symptoms. Pain is more indicative of stone than any other 
cause of obstruction of the common or cystic duct. Thus, in 80 cases 
of common-duct obstruction pain was marked in 51, absent in 10, 
and unrecorded in 19, while in 79 cases due to other causes than 
stone, pain was present in only 9. 

If the stone is movable, there may be attacks of acute radiating 



544 PAIN 

pain with chills, and sweats due to absorption of toxic matter through 
the abraded mucous membrane. (See Charcot's Fever.) 

Boas has pointed out that in many cases of gallstone a spot of 
tenderness may be found at the level of the twelfth dorsal vertebra 
three inches to the right of the vertebral line. 

Severe pain in the hepatic region may also be due to acute cholecys- 
titis. There is usually local muscular rigidity, tenderness, and vomit- 
ing, but the liver is not enlarged unless the cholecystitis is associated 
with cholangitis. This condition follows the infectious fevers, notably 
typhoid fever, and may be confused with appendicitis, which often 
causes cholangitis or abscess behind the liver. 

The pain of diffuse hepatitis varies with the severity of the inflam- 
mation, and it may not be present unless the hypochondrium is 
palpated. In cholangitis it is rare unless suppuration is localized, 
but in cholecystitis of a chronic type the pain often comes on in par- 
oxysms, and is associated with fever, enlargement of the gall-bladder, 
and great tenderness in its area on palpation. The liver itself is not 
enlarged. If suppuration is present, the symptoms of general sepsis 
may develop. The paroxysms of pain may vary like those of gall- 
stone in the endeavor of the gall-bladder to extrude its thick muco- 
purulent contents. Care should be taken not to mistake a subphrenic 
abscess for cholecystitis. 

When there is a history of violent colic situated near the hypochon- 
drium, or in the epigastrium, not accompanied by jaundice and 
enlargement of the liver, the possibility of the cause being a pan- 
creatic calculus is not to be forgotten. Such a condition is rarely 
met with it is true, and still more rarely do we find pancreatic stones 
in the feces, because they are friable and broken up in the feces 
before they are passed. Boas states that they are a frequent cause 
of so-called "neuralgia of the liver." It should not be forgotten 
that blocking of the common duct by gallstone also produces block- 
ing of the pancreatic duct, and this in time may cause a complicating 
attack of acute pancreatic necrosis. 

The pains just described are so severe and characteristic in their 
distribution that they cannot well be confused with those of intestinal 
indigestion, in which condition we have a history of the ingestion of 
bad food, a state of more or less flatulent distention of the entire 
belly, and, it may be, diarrhea. 

The pain arising from the presence of a gastric ulcer may, with its 
associated symptoms, so closely resemble that due to cholelithiasis 
as to make a differential diagnosis almost if not quite impossible. 
The same statement holds true of duodenal ulcer, but the comparative 
rarity of this lesion excludes it on the ground of improbability. The 
pain of all these affections may be so near the area of the biliary 
passages that its localization by the patient gives the physician no 



ABDOMINAL PAIN 545 

aid whatever. Jaundice is so often absent in cases of hepatic colic 
that its absence in no way excludes this state. While the presence of 
an excess of hydrochloric acid in the gastric contents points to ulcer it 
sometimes occurs that hyperacidity arises from reflex irritation from 
the gall-bladder. Even the development of pain a definite time after 
the ingestion of food, due to the irritating effect of the acid upon the 
gastric ulcer, may also develop in cases of gallstone if there has 
developed around or about the gall-bladder inflammatory exudations 
and adhesions which interfere with the movements of the pylorus 
and duodenum as the food passes into the small bowel. The pres- 
ence of hematemesis is strongly indicative but not pathognomonic of 
ulcer. 

Finally, the physician must bear in mind that occasionally severe 
abdominal pain with vomiting, diarrhea, and even the passage of 
blood maybe the result of angioneurotic edema with an abdominal 
crisis. This pain is usually diffused throughout the belly and not 
confined to one area although at onset it may be in the epigastrium. 
These symptoms may seriously mislead the surgeon unless he first 
makes inquiries, designed to discover the fact that attacks of angio- 
neurotic edema have affected other parts of the body. This is the 
more important in view of the fact that these attacks are often pre- 
cipitated by indiscretions in diet as is appendicitis and gallstone 
colic. The skin should always be carefully examined to discover 
traces of urticaria. 

The sudden development of pain of great intensity in the right 
lower quadrant of the abdomen (see McBurney's point, Fig. 202), 
associated with muscular rigidity of the abdominal wall, tenderness 
on palpation, a quick pulse, and in some instances vomiting indicates 
the development of appendicitis', a diagnosis which is aided, but not 
confirmed, if on examining the blood a distinct leukocytosis is pres- 
ent. It is worthy of note that the pain of appendicitis is often referred 
in its greatest intensity, and by intelligent patients, not to the neigh- 
borhood of the appendix, but to the epigastrium, or even to the 
region of the sigmoid flexure, and it is by careful palpation only that 
the area of greatest tenderness is found in the appendicular region. 

Before reaching a diagnosis of acute appendicitis the physician 
must exclude the following causes of pain referred by the patient to 
the appendicular area. One of these is diaphragmatic pleurisy; 
still another is subphrenic abscess and a fourth is ovarian or tubal dis- 
ease if the patient be a woman. Rarely a floating kidney may be 
provocative of similar symptoms as may also phlebitis of the iliac 
vein. If the pain is very severe, so severe that the patient is incapaci- 
tated from giving a clear description of its chief seat, it may be due 
to gallstones, renal stone, or intestinal perforation. Severe pain may 
also be due to inflammation or twisting of Meckel's diverticulum. 
35 



546 



PAIN 



Generally diffused pain of a constant severe character felt all over 
the abdomen or localized at first in some particular spot, and greatly 
increased by pressure, should lead the physician to examine the case 
for a possible peritonitis. Nothing else causes such violent, diffuse 
pain. The well-flexed legs, the anxious face, the drawn upper lip, 
quick pulse, the exquisitely tender abdominal surface, the .thirst, the 







Fig. 202. — The black spot is at "McBurney's point." 

moderate fever, and the rapid onset of collapse in fatal cases render 
the diagnosis easy. 

In pancreatitis the pain is sudden in onset, violent, and usually 
felt chiefly in the left upper zone of the abdomen. The belly is 
distended, nausea and vomiting are present, and fever may be 
present also; delirium may come on, and death generally speedily 
ensues unless operative measures are resorted to. (See Abdomen.) 

The onset of severe pain in the abdomen in the course of typhoid 
fever, while not necessarily an indication of perforation of the bowel, 



ABDOMINAL PAIN 547 

is nevertheless deserving of careful study. If it is due to perforation, 
as a rule it is violent enough to make the patient cry out if he be not 
stuporous, and the following symptoms will probably be present in 
whole or in part: The epigastrium and general abdominal wall will 
be fixed; the abdominal wall may be scaphoid or distended, but is 
usually hard. Percussion of the area of the liver may show oblit- 
eration of hepatic dulness, as a result of gas being between the wall 
and this organ, but while this is an important sign if present, its 
absence does not exclude perforation. Hiccough may be present, and 
perhaps vomiting. The facial expression is that of grave abdominal 
disorder. (See chapter on the Face.) An examination of the blood 
may show leukocytosis, and if such an increase in white cells is pres- 
ent, it is an important positive factor in confirming the diagnosis of 
perforation. An absence of leukocytosis not only does not negative 
the diagnosis of perforation but it may confirm it, because if the 
shock be great leukocytosis may be prevented by the very intensity 
of the insult to the peritoneum. As in suspected appendicitis so in 
suspected typhoid perforation, the chest must be carefully examined 
lest the pain of an acute pleurisy be mistaken for abdominal 
disorder. So, too, it is essential that the pain of acute cholecystitis, 
appendicitis, and renal calculus be excluded before a diagnosis of 
perforation is determined. 

Severe abdominal pain in typhoid fever may, however, be the 
result of wind colic, acute pleurisy, a distended bladder, cholecystitis, 
and impaction of feces. 

Sometimes a patient who has floating kidney will suffer from severe 
renal pain, nausea, vomiting, and collapse, the symptoms simulating 
renal calculus. These attacks are known as Dietl's crises. 

If the pain be due to chronic lead poisoning, it centres about the 
umbilicus, and is of a twisting, knotty character, "as if the bowels, 
were being twisted around a stick." There is a history of exposure 
to lead in many cases, and a blue line on the gums can often be 
found. 

If due to fecal impaction, there is a history of a continued tendency 
to constipation, with dry, hard stools, and a lump of hardened feces 
may perhaps be felt through the belly wall. 

If due to intestinal obstruction, the pain has no characteristic seat 
in any part of the abdomen, as a rule; but the general symptoms of 
this condition will be found present in the case. (See chapters on 
Vomiting and on the Abdomen.) 

Abdominal aneurysm may cause severe pain by pressure on nerve 
trunks; and uterine and peri-uterine disease also cause, reflexlv, 
epigastric pains. 

Reference has already been made to the pain of renal colic. The 
characteristic symptoms of this condition are as follows: In renal 



548 PAIN 

colic the patient is suddenly seized with violent pain in the region of 
the kidney on one side, which passes down to the groin and even to 
the end of the penis. It is paroxysmal in character, and so excessively 
severe that it often produces sweating, vomiting, and even fainting. 
The condition is seen much more frequently in men than in women. 
The pain often suddenly subsides, leaving only a sense of soreness 
and tenderness in its track. The urine may be partly suppressed and 
bloody if the stone injures the ureter to any great extent. Pain 
simulating renal colic may be due to neuralgia or arise from several 
organic causes not connected with calculus. Thus, Habershon has 
stated that in valvular disease of the heart, particularly of the aortic 
valve, severe and colicky pains frequently radiate down into the right 
hypochondriac region, and Ralfe says into the renal region. Again, 
pain in this part may be due to aneurysm of the aorta or of the mesen- 
teric artery. Further, the accumulation of hard fecal matter in the 
colon may cause nephralgia. Finally, Ralfe calls attention to the 
renal pain felt generally in the right kidney by women who have 
exercised violently while wearing a tight corset, which has pressed 
upon the liver and kidney with great force on making a jump or 
a sudden bend of the trunk. Sometimes a sudden " storm" of uric 
acid or an accumulation of oxalic acid in the kidney causes pain 
and tenderness. 

The presence of constant pain and soreness in the abdomen on 
one side, frequent micturition, and occasionally the presence of 
blood in the urine, are symptoms of several renal states, such as 
pyelitis, renal calculus, a tumor in the renal pelvis, and tuberculosis 
of the kidney. The pain is chiefly in the region of the kidney and 
along the course of the ureter where it crosses the pelvic brim; and 
as it is often made more severe by standing and is of a bearing-down 
character, it may be thought in women to be uterine. Jolts or jarring 
of the body also aggravate it, as does the act of urination. Sometimes 
a good deal of pain is felt on the sound side. 

If an examination of the urine reveals pus, this will indicate pye- 
litis; and if the pus contains tubercle bacilli, tuberculous pyelitis. 
The latter diagnosis is confirmed if tuberculous disease is present 
in other organs, for renal tuberculosis is usually secondary. Small 
cheesy masses may be present in the urine in the latter state. 
Renal calculus will be attended by attacks of renal colic, which, as a 
rule, are more severe than those produced by the passage of masses 
of broken-down matter along the ureter. A history of having passed 
a stone at some previous time, and the discovery of blood corpuscles 
in the urine are of importance in the diagnosis. 

Pain in the abdomen of the darting neuralgic type, other than that 
due to gallstones, renal calculi, ordinary gastralgia, lead poisoning, 
enteralgia, or malignant growth, may be due to locomotor ataxia. 



ABDOMINAL PA1X 



549 



This possibility should never be forgotten, and the fact that the 
patient is an adult, complains of the most violent pain in the belly, 
and has no other abdominal signs, should make us search for the 
other signs of tabes dorsalis. Generally these attacks will be of a 
tearing, rending character; they may be beyond description in 
severity, and after they pass off the patient is left in a condition of 
nervous wreck. Sometimes the pain is in the stomach, sometimes 
in the bladder. 

Some Abdominal Conditions en which Sudfen and Acute Pain fobmb a 
Prominent Symptom. 1 



Disease. 



Mode of 
onset. 



Character of pain. 



Acute intestinal 
obstruction : 
a. Strangula- Very sud- 
tion due to den. 
bands. 



In kind. 



More or less 
continuous. 



b. Acute intus- 
susception. 



Sudden Paroxysmal. 

to very 

sudden. 



c. Acute volvu- Sudden, 
lus. 



d. Due to gall- Less sud- Paroxysmal 
stone or \ den, gra- later, 
stricture. dual, j 



Paroxysmal, 

but less than 

b. 



Appendicitis. 



Very sud- Quite con- 
den, tinuous. 



In inten- 
sity. 



Most in- 
tense, 
agonizing. 

Severe. 



Moderate. 



Moderate. 



Seat of pain. 



Epigastric or um- 
bilical region. 



Epigastric or um- 
bilical region. 



Umbilical or over 
heart. 



Often near seat of 
obstruction. 



Tenderness and 
pressure. 



Pressure at first re- 
lieves, afterward 
aggravates. 

Pressure at first re- 
lieves, afterward 
aggravates. 

Pressure never 
causes pain. 



Tenderness over 
obstruction. 



At first periumbili- 
cal, later about 
appendix. 



Agonizing. At first periumbili- Greatest over ap- 
pendix or in left 
groin. 

Acute peritonitis. Very sud- Continuous. Very severe All over belly, but Very tender every- 
d'en. I chiefly epigastric where except at 

or umbilical. very first. 



Hepatic colic. 



Renal colic. 



Intestinal colic. 



Sudden. Aching, tear- Agonizing. 
| ing, parox- 
ysmal. 



Sudden. 



Aching, tear- 
ing, parox- 
ysmal. 



Epigastric, radi- 
ating to between 
shoulders or to 
shoulder-blade. 



Agonizing. Affected loin, pass- 
ing down in front 
into testicle and 
bladder. 



Pressure at first re- 
lieves, then un- 
bearable over 
gall-bladder. 

Tenderness over 
affected kidney. 



Sudden Paroxysmal. Varies in Varies in position. Relieved by press- 
or severity. ure. 
gradual. 



Grube has recently reported cases showing that diabetes may pro- 
duce attacks of violent abdominal pain resembling the crises of an 
ataxia. 

Neuralgic pain in the back and abdominal parietes very closely 
resembling, if severe, renal or hepatic colic is sometimes due to 
gastralgia, the paroxysms being very sudden in onset. In other 



Andrews' table, slightly modified. 



550 PAIN 

instances the pain is in the epigastrium or hypogastrium, and is 
associated with so much tenderness on light pressure as to impress 
the careless with the belief that gastric ulcer or cancer is the cause. 
Neuralgic spots can generally be isolated in such persons if the skin 
is carefully tested for its degrees of sensation, and these spots will be 
found to exist near where the nerves are given off from the spine or 
over the spine of the ilium. In some of these cases the cause of 
the so-called gastric pain really exists in the presence of otherwise 
quiescent gallstones. 

Circumscribed abdominal pain of a constant character and gen- 
erally of less severity than that just described, may be due to an 
abdominal tumor (see Abdominal), or to ulcer of the stomach or 
bowel. 

In dysmenorrhea the pain is sometimes so severe as to render the 
patient almost insane, but it differs from that of inflammation in that 
it is paroxysmal and that there is no real tenderness on pressure; 
and, again, the patient does not lie still, but tosses from side to side 
in the bed. The pain of pelvic tumor is usually produced by 
pressure on a nerve, and is increased by palpation in some cases, 
as is also that of ovaritis. In cystitis the pain is deep in the 
pelvis, radiating upward, and is associated with tenderness, vesical 
spasm, and tenesmus. 

The pain of fissure of the anus is not at all proportionate to the 
lesion producing it. This pain may be atrocious and agonizing, and 
often is produced by a movement of the bowels, after which it lasts 
for some hours. 

(For abdominal pain due to conditions associated with movements 
of the bowels, see chapter on the Bowels and Feces.) 

Pain in the Feet and Limbs. — Neuralgia of the toe and foot is 
not a very rare condition, and is sometimes called " Morton's painful 
toe," or metatarsal neuralgia. Severe pain at the base of the fourth 
toe comes on suddenly, and may radiate up the anterior aspect of the 
leg. Sometimes it is only dull, at other times it is so sharp and excru- 
ciating as to cause the patient to scream. It is separated from gout 
by the absence of any signs of inflammation in the part, by the fact 
that the big toe is not affected, and by the age and history of the 
patient. At times the base of the second toe is affected. Such a case 
will usually indicate that the patient has worn an ill-fitting boot. 

Finally, in connection with this class of cases there should not be 
forgotten two others, namely, those in which idiopathically or other- 
wise, growths form on nerves and cause pain; and, secondly, cases 
in which the arm or leg having been amputated, a neuroma, or catch- 
ing of the end of the nerve in the scar, causes violent pain in the lost 
part, according to the patient's sensation, because the perceptive 
centres have been trained to regard pain impulses coming along this 



PAIN IN THE FEET AND LIMBS 551 

nerve as from its peripheral end. Thus a man whose leg may have 
been amputated years before will complain of severe pain in the 
amputated foot, although he knows it is off. 

Pain in the back is often very severe in the early stages of smallpox, 
of epidemic influenza, and in lumbago. 

One of the most misleading forms of pain of a severe character, 
involving the entire body, with fever, delirium, and a variable skin 
eruption and swelling of the joints, may in the early stage he thought 
to he smallpox or rheumatic fever, when in reality it is due to dengue 
or breakbone fever. 



CHAPTER XXL 

TENDON REFLEXES AND MUSCLE TONE, 

The knee-jerk and ankle-clonus — The arm-jerk — The significance of decreased 
and increased reflexes. 

We have already had occasion, particularly in those chapters 
devoted to the Legs and Feet and the Arms and Hands, to speak 
of what are called the reflexes or "muscle-jerks." There is much 
discussion as to whether the muscular contractions produced by tap- 
ping the tendon attached to a muscle are the result of a reflex action, 
in which the spinal cord is directly involved, or whether it depends 
upon muscle irritability or tone. It is not necessary for purposes 
of diagnosis to enter into a discussion of this character, because the 
facts in our possession prove conclusively that variations in these 
muscle-jerks are of great diagnostic importance in diseases of the 
nervous system, whether they be true reflexes or not. The knee-jerk, 
or, as it has been called, the patellar reflex, is the diagnostic sign 
most frequently sought in studying nervous diseases associated with 
lesions in the spinal cord, because it is most easily developed. 

The methods of developing the knee-jerk, elbow-jerk, and ankle 
clonus ha\e already been described in the chapters on the Hands 
and Arms and the Feet and Legs, to which the reader is referred. 

The chin-jerk is elicited by having the patient open his mouth 
slightly and then placing a flat object, like a paper cutter or tongue 
depressor, on the edges of the lower teeth. A sharp tap is now given 
to the flat object, when in health there will be a slight upward jerk 
of the chin. 

The scapulohumeral reflex of von Bechterew is elicited by tapping 
the skin on the spinal border of the scapula near its inferior angle. 
This usually causes a slight adduction and external rotation of the 
arm. It is exaggerated in neurasthenia, but its chief diagnostic value 
is in connection with lesions in the pyramidal columns above the 
cervical enlargement, in which state it is greatly altered in that we 
now find contraction of the posterior fibers of the trapezius, the del- 
toid, biceps, and forearm mucsles, so that the shoulder is raised, the 
arm thrown from the side, the forearm flexed, and the fingers ex- 
tended that the muscles on the opposite side also respond. If the 



TENDON REFLEXES AND MUSCLE TONE 553 

brachial plexus be diseased, the response on that side may be greater 
than on the side that is tapped. 

Having learned how to test these muscle-jerks, we now turn 
to a consideration of what they mean when absent or abnormally 
increased. 

A loss of knee-jerk is not characteristic of any disease unless this 
loss is associated with other symptoms which only need the discovery 
of this symptom to confirm the diagnosis. The nervous conditions 
in which we find the reflexes decreased or lost, taking the patella 
reflex as a type, are locomotor ataxia; peripheral neuritis; polio- 
myelitis, acute or chronic; transverse myelitis, if the disease involves 
the reflex arc; Friedreich's ataxia; diphtheritic paralysis; apoplexy, 
immediately after the shock; Landry's paralysis; spinal meningitis; 
spinal injuries, immediately after the accident; epilepsy, immediately 
after an attack ; and chorea. We also find a total loss of reflexes in 
advanced diabetes mellitus and sometimes in diabetes insipidus. 

By far the most common cause of the loss of the knee-jerk is loco- 
motor ataxia, but any lesion involving the posterior columns of the 
cord or the posterior nerve roots in the second, third, or fourth lum- 
bar segment will produce the same results. Therefore, loss of knee- 
jerk is symptomatic of transverse myelitis of this region as well as of 
ataxia. Again, if the motor tract of the cord at these levels is dis- 
eased the knee-jerk is lost, as, for example, in acute and chronic 
poliomyelitis or myelitis involving the motor part of the reflex are; 
and, finally, peripheral neuritis, which blocks the pathway from the 
periphery to the cord, and from the cord to the muscles, also causes 
loss of knee-jerk. 

If the cause of loss of knee-jerk be locomotor ataxia, we will 
probably find in addition to this symptom some difficulty in walking, 
particularly if the eyes are shut; a lack of steadiness if the feet are 
placed together when the patient stands with his eyes shut; Argyll- 
Robertson pupils, or a reaction to accommodation but not to light; 
attacks of severe pain in the body or limbs; and, it may be, laryngeal 
crises or spasms and atrophy of the optic nerve. 

If the cause of loss of knee-jerk be neuritis, we will find tenderness 
on pressure along the nerve trunks, diminished muscular tone, 
and some wasting; an absence of any disturbance of the bladder 
and no Argyll-Robertson pupil, laryngeal or other crises, nor 
optic atrophy. 

Again, if the cause be acute poliomyelitis, there will be a history 
of sudden onset with fever, the limbs will be relaxed and flabby, 
the muscles will rapidly waste and become very feeble or paralyzed, 
and there will be no sensory symptoms whatever. The patient will 
usually be a child if the disease is acute. If the loss be due to trans- 
verse myelitis of the second, third, and fourth lumbar segments, 



554 TENDON REFLEXES AND MUSCLE TONE 

the symptoms of paraplegia, parasthesia, and anesthesia, with 
atrophy of the muscles and loss of control of the bladder and rectum, 
will be present, and a girdle sensation may be marked. 

In Friedreich's ataxia the history of heredity, the nystagmus, 
the early age of the patient, the absence of pupillary symptoms, the 
ataxic gait, and the loss of reflexes, are the facts which go to form our 
basis for a diagnosis. In the remaining diseases named the history 
of the case points to the cause of the loss of the knee-jerk very clearly. 

The conditions in which we find the knee-jerk increased are 
apoplexy after the attack; disseminated sclerosis; cerebral palsy 
of childhood; paretic dementia (not constant); primary lateral scle- 
rosis; amyotrophic lateral sclerosis; ataxic paraplegia; hysterical 
paraplegia; transverse myelitis if the lesion is above the reflex arc; 
epilepsy some minutes after the attack; unilateral lesions of the 
cord on the paralyzed side; injuries to the spinal cord, after the 
recovery from first shock; pressure on spinal cord alove the reflex 
arc; hereditary cerebellar ataxia; sciatica; tetanus; rheumatoid 
arthritis; and neurasthenia. 

The history of sudden paralysis and unconsciousness in a case of 
apoplexy with stertorous breathing, followed by loss of the knee-jerk, 
and then its return in an exaggerated manner, make the diagnosis 
clear unless the attack be one of the apoplectiform attacks of dis- 
seminated sclerosis, in which case there will be present a history 
of the intention tremor, nystagmus, and the syllabic speech, so that 
though the knee-jerk is exaggerated in both diseases the diagnosis 
can be readily made. In the cerebral palsy of childhood the age of 
the patient, the contractures and gait, with the history, decide the 
diagnosis. In lateral sclerosis the spastic rigidity, excessive exag- 
geration of the knee-jerks, absence of sensory disturbances, and 
ocular symptoms, all render the diagnosis possible. Similar exag- 
geration is also seen in amyotrophic lateral sclerosis, in which disease 
there is wasting of the muscles, particularly of the hand. In both, 
these ailments the exaggeration of the knee-jerk is due to disease of 
the lateral pyramidal tracts, which block the inhibitory fibers from 
the higher centres. For similar reasons we find exaggerated knee- 
jerk in ataxia paraplegia. 

In hysterical paraplegia the age and sex of the patient, the peculiar 
facies, the areas of anesthesia and hyperesthesia, and the peculiar 
gait point to the diagnosis. 

The increased knee-jerk in cases of transverse myelitis occurs 
when the lesion is situated at such a point in the cord that the lateral 
tracts are cut off and the reflex arc is preserved. 

In neurasthenia the knee-jerks are exaggerated, but are easily 
exhausted. 

Leaving the knee-jerks as a type of a reflex, we find that the skin 



TENDON REFLEXES AND MUSCLE TONE 555 

reflexes are often lost in eases of apoplexy when the deep reflexes 
are exaggerated. The table on page 78, from Taylor's Index of 
Medicine, shows the area of skin reflexes very well. 

The plantar reflex obtained by tickling the sole of the foot has 
recently attained considerable diagnostic importance through the 
work of Babinski, who has found that in normal persons such irrita- 
tion causes flexion of the toes on the metatarsus, whereas in disease 
of the pyramidal tracts extension of the great toe, with or without 




Fig. 203. — Babinski reflex in health, somewhat exaggerated. The toes are drawn 
up toward the knee. 

extension of the other toes, takes place, as, for example, in spastic 
paraplegia. The normal reflex, somewhat exaggerated, is shown in 
the figure. It is a noteworthy fact that in infants in health extension 
takes place instead of flexion, and that the administration of full doses 
of strychnine to adults will sometimes reverse the normal reaction. 
The Babinski reflex is not pathognomonic of disease of the pyramidal 
tract, although it is indicative. 

In glossolabiopharyngeal paralysis the reflexes of the tongue and 
throat are lost and those of the face sometimes increased; in pro- 
gressive muscular atrophy the reflexes of the arms are lost, while 
those of the legs are preserved; and in tuberculous meningitis the 
reflexes are apt to be more marked on one side than the other. 

In athetosis the reflexes are increased in the affected part. 

Ankle clonus is found most marked in lateral sclerosis, in dissemi- 
nated sclerosis, and in amyotrophic lateral sclerosis. A false clonus 
is sometimes seen in hysteria. 



556 



TENDON REFLEXES AND MUSCLE TONE 
A Table of the Eeflexes. 



Reflex. 


Point of stimulation. 


Situation of centre. 


Significance. 


1. Plantar, 


Irritating skin of soles. 


Extreme end of cord. 


Usual in health. 


2. Gluteal, 


Irritating skin of but- 
tocks. 


Origin of 4th and 5th 
lumbar nerves. 


Rare in health. 


3. Cremasteric, 


Irritating skin of inner 
side of thighs. 


Origin of 1st and 2d lum- 
bar nerves. 


Usual in health ; best 
marked in boys, on 
account of the newly 
formed cremaster. 


4. Abdominal, 


Irritating skin of abdo- 
men in line of nipples. 


Origin of 8th to 12th dor- 
sal nerves. 


Frequently absent. 


5. Epigastric, 


Irritating skin of chest 
In 5th and 6th spaces. 


Origin of 4th to 6th dor- 
sal nerves. 


May be absent in health. 


6. Erector spinse, 


Irritating skin from sca- 
pula to crest of ilium. 


Origin of all the dorsal 
nerves. 


Rare in health ; frequent 
in wasting disease. 


7. Interscapular, 


Irritating skin between 
scapula?. 


Origin of 6th cervical to 
3d dorsal. 


Rare in health. 


8. Palmar, 


Palms of hands. 


Cervical bulb. 


Only in infants. 


9. Cranial: 

Conjunctival, 


Sclerotic, or inner sur- 
face of eyelid. 


Medulla. 


Absent in disease of 5th 
nerve only. 


Iris (to light), 


Pupil. 


Anterior portion of ocu- 
lomotor nucleus. 


Absent in disease only. 


Palate, 


Soft palate and uvula. 


Medulla. 


Absent in disease only. 


Nasal (sneez- 
ing), 


Naso-respiratory pas- 
sages. 


Medulla. 


Absent in disease only. 



CHAPTER XXII. 

SPEECH. 

The changes in the speech and voice — Their significance — Aphasia — Apraxia — 

Alexia — Paraphasia. 

The character of the speech and the tones of the voice often convey 
a considerable amount of diagnostic information to the physician. 
While in many diseases no marked alterations from the normal 
manner of speech are present, in others marked changes take place. 
Thus, in acute laryngitis due to exposure to cold or irritant vapors 
the patient has a ivhispering voice. In persons suffering from pul- 
monary tuberculosis the development of hoarseness and whispering 
or labored speech tells us only too well of the fact that the grave and 
distressing complication called laryngeal tuberculosis has arisen, and 
that the progress of the case will be more rapid toward the fatal result. 
Again, the sudden onset of whispering voice or complete aphonia 
occurring in a young girl whose facies is hysterical, should always 
arouse a suspicion of hysteria, while if the signs of this condition are 
absent and the patient has none of the signs of tuberculosis, we should 
examine the larynx for a papillomatous growth. Again, if hoarseness 
or a whispering voice is manifested by a male of adult years, who is 
also suffering from dyspnea, unilateral flushing or sweating of the 
face and neck, and unequal, rapid radial pulses, we should suspect 
aortic aneurysm or a mediastinal tumor which is pressing on his 
recurrent laryngeal nerve. There are also other causes of hoarseness 
due to nervous lesions arising from the long and tortuous course of 
the nerves supplying it. These have been well grouped together by 
Felix Semon. (See Table on next page.) It is interesting to note that 
in suspected cases of disease of the parts herein named it is well to 
make a laryngeal examination, since this may reveal a paralyzed cord, 
although the voice has not indicated such a condition, because by 
great retraction of the opposite cord the laryngeal opening is kept 
patulous and phonation is possible. 

Hoarseness may also be due to tuberculous infection of the larynx, 
to laryngeal papilloma, and hysteria. 

Hysterical mutism may occur in both males and females. It 
usually follows a fright or violent emotion, or it may follow an hysteri- 
cal seizure. Sometimes it develops without any such history. The 
condition lasts from a few hours to months or vears, and recovery 



558 



SPEECH 



is often as sudden and unsuspected as the onset. As a rule, the 
tongue, lips, and jaws are unimpaired in their functions. Some- 
times, however, these parts are affected by hysterical spasm. Often 
there will be hysterical anesthesia with the mutism. Usually there 
is no evidence of cerebral lesion in such cases in the sense of impair- 
ment of intellect. 
Table Showing the Possible Causes of Laryngeal Paralysis. 



I. Bulbar and Bulbospinal Affections. 

1. Hemorrhage and softening. 

2. Syphilitic processes. 

3. Tumors. 

4. Diphtheria. 



5. Progressive bulbar paralysis. 

6. That curious form of systemic central 
nervous disease first described by Hughlings 
Jackson and Morell Mackenzie, in which one- 
half of the tongue, the corresponding half of 
the palate, the corresponding vocal cord, 
and, in a number of cases, the corresponding 
trapezius and sterno mastoid muscles are 
affected. 

7. Amyotrophic lateral sclerosis. 

8 Disseminated cerebro-spinal sclerosis. 
9. Syringomyelia. 
10. Tabes dorsalis. 



II. Peripheral Affections. , 

1. Acute rheumatic influences. 

2. Catarrhal neuritis. 

3. Toxic influences (lead, arsenic, etc.). 

4. Tumors in the posterior cavity of the 
skull or in the foramen lacerum or foramen 
jugulare. 

5. Pachymeningitis. 

6. Traumatism (unintentional ligature of 
nerves, injection of iodine into a goitre, cut 
throat, stabbing, injury during extirpation of 
goitre, etc.). 



7. Tumors of neck (goitre, peritracheal 
glands, etc.). 

8. Aneurisms of the arch of the aorta, in- 
nominate, subclavian, carotid. 

9. Mediastinal tumors (malignant, tubercu- 
lous, calcification of bronchial glands, etc.). 

10. Pericarditis. 

11. Pleurisy. 

12. Tuberculosis and pleuritic thickening of 
apex of right lung. 

13. Chronic pulmonary affections (chronic 
pneumonia, anthracosis, etc.). 

14. Infectious fevers (typhoid, etc.). 

15. Oesophageal carcinoma. 



When a child speaks with a nasal twang or indistinctly we suspect 
the presence of adenoid vegetations, and will probably find that he 
or she is addicted to mouth breathing. Stuttering or stammering 
may also be due to this cause. 

A feeble, hesitating speech is often a sign of exhausting disease, and 
a short and quick but feebly spoken sentence generally indicates 
that the patient is suffering from some cardiac or pulmonary com- 
plaint, which renders him short of breath, so that he hurries through 
the sentence in order to be able to breathe freely again. In cases of 
pneumonia or of pulmonary edema this hurried speech is a very 
characteristic sign. 

Again, in cases of typhoid fever, when the tongue is dry and 
immobile from accumulated sordes, a mumbling character of the 
speech is present, even if the brain is entirely clear, and in severe 
stomatitis the same quality of the voice may be present. 



APHASIA 559 

It is in connection with the disorders of the nervous system, how- 
ever, that the most typical alterations of the voice occur. Let us 
suppose that a patient in middle life or in more advanced years 
develops a slow, scanning speech, with intention tremors (see chapter 
on the Hands), nystagmus, and more or less muscular weakness. In 
all probability he is a sufferer from insular or, as it is otherwise called, 
disseminated sclerosis. When he speaks each syllable is sharply 
accentuated and slowly pronounced. The only other condition in 
which a slow, scanning speech is of great diagnostic importance is 
in that rare disease Friedreich's ataxia; but the facts that this 
disease begins in childhood, that several members of the family 
are apt to be affected, that there are ataxic symptoms and early 
talipes equinus, render it easy to separate this affection from insular 
sclerosis. (See Paraplegia, in chapter on the Feet and Legs.) 

A hesitating, halting speech associated with Argyll-Robertson 
pupils, unequal pupils, delusions of grandeur, and tremor of the 
tongue, which last symptom may be so marked as to cause the speech 
to be indistinct and blurred, is indicative of paretic dementia. 

If an incoherent speech develops in a child who is not suffering 
from an acute illness causing delirium, there" will usually be found 
in association with this symptom the nervous twitchings of chorea, 
for speech disturbances occur in about one-third of the patients 
suffering from this disease. 

A very indistinct speech of a mumbling character, great difficulty 
being experienced in the pronouncing of dental and lingual sounds, 
and perhaps associated with feebleness of the voice, if the larynx is 
involved, is seen in cases of glossolabiopharvngeal paralysis. If 
the cause of the defective speech be this disease there will be found, 
as associated symptoms, wasting of the tongue, lingual tremors, sonic 1 
dribbling of saliva from the mouth, and immobility of the lips, the 
face about the mouth being expressionless. 

Somewhat similar symptoms due to paralysis of the lips, with 
escape of the tongue and pharynx, at least for a long time after 
labial paralysis develops, are sometimes seen in advanced cases of 
amyotrophic lateral sclerosis; and a still more close resemblance 
may be produced by the so-called "pseudobulbar paralysis," the 
lesion of which is in the motor cortex of the brain on 1 oth sides, in 
the lower part of the ascending frontal convolution. Rarely the 
latter is only a unilateral disease. 

A rather shrill, piping voice, the sentence being begun with hesi- 
tation and then hurried to an end in a rapid volley of words, is some- 
times seen in paralysis agitans. 

Aphasia. — By far the most interesting speech defect is that 
called aphasia. It is divided into motor aphasia and sensory 
aphasia. 



560 SPEECH 

Before studying these conditions we must discuss the nervous 
mechanism of speech. When a child learns to talk it performs a 
purely imitative act. Its auditory nerve conveys the sound to its 
perceptive centres, and from here an impulse is sent to its motor 
speech centres, and these again send impulses to the inferior speech 
nuclei in the medulla oblongata, which in turn move the muscles of 
speech. Simultaneously the child learns the words and stores them 
in memory centres for sounds, and also stores in memory centres 
"motor memories/' which tell him how to repeat the muscular 
movements a second time. Again, when he learns to recognize 
objects and call them by name he must use "visual memory" centres. 
These centres are all best developed in the left hemisphere of the 
brain in right-handed persons and in the right half of the brain in 
left-handed persons. 

If a person suffers from pure aphasia, he simply loses the memory 
of how to say certain words, and the lesion is in the third left frontal 
(Broca's) convolution. This state is sometimes called aphemia. 
The patient knows what a knife is when he sees it, but he cannot 
recall his motor memories so as to move the muscles to say "knife." 
He can read to himself, because he has not forgotten the meaning of 
the words, and for this reason he understands what is said to him, 
and may be able to repeat a word immediately after it is said, by a 
purely imitative process. Generally, we find with aphasia a condition 
called agraphia, in which the patient cannot write his thoughts, but 
can copy perfectly. In the great majority of cases of aphasia, how- 
ever, the patient is paralyzed in his right hand, so that the symptoms 
of agraphia cannot be demonstrated. Under the name of paraphasia 
we sometimes meet with a condition in which the patient can speak 
quite freely, but transposes words or interpolates useless words to 
such an extent that what he says is unintelligible. When the patient 
slips words, the lesion is in the associating tracts between the speech 
centres, and this is called conduction aphasia. 

In another condition closely connected with aphasia we have a 
state in which the patient can spell out words from a page set before 
him, but he cannot read, because the words convey no idea to him. 
This is called alexia, or "word blindness." Again, he may forget 
the use or significance of certain objects, such as a knife and fork; 
this is called apraxia. Still further, words when spoken to the patient 
in his native language may be heard perfectly, and yet understood 
no more than if in some unheard-of language. This is called "word 
deafness." 

If the patient has simple aphasia he has a lesion in the third 
frontal convolution in its posterior part. If he has word blindness 
or alexia, the lesion is in the angular gyrus, extending back into 
the occipital convolution. If he has apraxia or the loss of memory 



APHASIA 5(31 

of objects, the lesion is in the same area as in alexia; and if "word 
deafness" is present, the lesion is in the posterior part of the first 
temporal and upper part of the second temporal convolution of the 
left hemisphere. As the various symptoms of aphasia in all its forms 
are closely associated with those of focal lesions of the brain, resulting, 
for example, from hemorrhage or embolism, the reader should read 
the chapter on Hemiplegia in this connection. 

Aphasia is quite frequently met with as a symptom of hysteria, and 
may occur independently of any organic lesion, so far as we know, in 
children during convalescence from an attack of a severe infections 
disease. Tn the latter cases speech may return many months after. 

The following plan of testing a patient, devised by Eskridge from 
a shorter one by M. Allen Starr, may be followed with advantage: 

1. The power to recognize objects seen, heard, felt, tasted, smelt, 
and their uses. 

2. The power to recall the spoken names of objects seen, heard, 
felt, tasted, and smelt. 

3. The power to understand sounds other than speech. 

4. The power to understand speech and music. 

5. The power to call to mind objects named and point them out 
at request. 

6. If word-deaf, can he recognize his own name when it is spoken ? 

7. The power to recognize a word spelled aloud. 

8. The power to call up mentally the sound of a note, figure, 
letter, or word. 

The examination thus far will test the various sensory areas, but 
more especially the auditory and the association tracts between the 
different sensory areas connected with speech. 

9. The power to recognize letters, figures, notes, and colors seen. 

10. The power to understand printed and written words seen. 

11. The power to read printing, writing, and music aloud and 
inaudibly, and to understand what he reads. 

12. The power to recall objects, the names of which are seen. 

13. The power to write voluntarily. 

14. The power to write at dictation. 

15. The power to copy, and the manner of copying, printing, and 
writing. 

16. The power to write the names of objects seen, heard, felt, 
tasted, and smelt. 

17. The power to read aloud and inaudibly, and to understand 
what has been written. 

18. The power to write his name and the ability to read it when 
written by himself and by another person, or when it is printed. 

19. The power to recognize a letter by tracing it with the index 
finger or with a pencil, the movements being guided by another, 

36 



562 SPEECH 

20. The power to call up mentally the appearance of an object, 
a figure, a note, letter, or word, when word-blind. 

These additional tests will aid in determining the condition of the 
visual word memories in the angular gyrus, and the connection 
between this area and the surrounding sensory and motor areas. 

21. The power to speak voluntarily, and, if impaired or lost, the 
character of the defect. 

22. The power to repeat words after another. 

23. Does the patient recognize his mistakes in speaking and 
writing, and can he correct them ? 

24. Can the patient think in speech (propositionize) ? 

25. Is there any special difficulty in the use of nouns, verbs, or 
other parts of speech ? 

26. The power to understand pantomime or gesture expression. 

27. The power to employ intelligently gesture in expression. 

28. The power to read figures and to calculate. 

29. The power to count both money and in numbers. 

30. The power to play a game of cards or other games. 

It is not to be forgotten that speechlessness is often present in 
melancholia and dementia. Further, temporary speechlessness or 
apparent aphasia may follow severe typhoid fever as a result of cor- 
tical exhaustion without the development of hemorrhage, embolus, 
or thrombus. The prognosis is favorable. 






INDEX. 



Abadie's sign, 27 

Abdomen, 279 
distention of, 281 
frog belly, 280 
inspection of, 280 
localized bulging of wall of, 285 
pain in, 13, 542-549 
palpation of, 287 
percussion of, 287 
"phantom tumor" of, 309 
regions of, 280 
scaphoid, 281 

swelling in epigastrium, 285 
tumors of, 289 

position in, 5 
wall, protrusion of, 280 

retraction of, 287 
Abscess, cerebral, character of pain in, 

539 
choked disk not generally present in, 

439, 510 
coma in, 489 
diagnosis of, 510 
fever in, 510 
gangrene in, 157 

symptoms of, 476, 489 

tache eerebrale a sign of, 144 

vomiting in, 509, 510 
hepatic, brick-dust sputum in, 529 

dysentery a cause of, 459 

fever in, 457 

hiccough in, 508 

pain in, 544 

sweating in, 457 

sjrniptoms and signs of pvemic. 
303 
of tropical, 303 

tongue in, 116 

vomiting in, 522 
lumbar, sciatic pain in, 541 
mastoid, edema back of ear in, 

164 
mediastinal, acute, historv in, 243 

cold, 243 

diagnosis of, 243 

purulent sputum in, 530 
of pancreas, 305 
perinephritic, 309 



Abscess, pulmonary, chronic morning 
cough in, 526 
copious and purulent sputum in, 

232, 530 
diagnosis between mediastinal 

growths and, 243 
elastic fibers in sputum of, 532 
following amebic dysentery, an- 
chovy-sauce sputum in, 530 
history, signs, and svmptoms of, 

231, 232 
rapidity of respiration in, 200 
pyopneumothorax subphrenicus, 305 
renal, pus-casts in multiple, 346 A 
retro-esophageal. See Retroesopha- 
geal abscess, 
subphrenic, purulent sputum in, 530 
Accommodation, pupillarv reaction to, 

426 
"Accoucheur's hand" in tetany, 45, 504 
Acetonuria, 364 

Oppenheimer's modification of Den- 
nige's test for, 365 
Acne due to bromine or iodine, 151, 152 
to iron, 152 

to working in paraffin, 152 
of forehead, purulent, in syphilis, 153 
Acromegaly, enlargement of feet in, 
88 
of tongue in, 121 
face of, 17 
head in, 30 

spade-like hand in, 40 
Acroparesthesia, 187 

diagnosis of, 187 
Actinomycosis, actinomvces in sputum 
of, 533 
as a cause of empyema, 239 
enlargement of tongue in, 121 
Acuity of vision, changes in, 429 
Addison's disease, coma in, 490 
convulsions in, 503 
heart in, 264 

pigmentation of buccal mucous 
membrane in, 128, 264 
of skin in, 137, 264 
symptoms of, 137 
tongue in, 117 
Adherent pericardium, svmptoms of, 
204 



564 



INDEX 



Adhesive pericarditis, symptoms of, 

302 
Adipose dolorosa, 164 
Adolescence, albuminuria of, 359 
Agraphia, 560 

location of lesion in, 560 
Ainhum, 95 

Air passages, foreign bodies in, 242 
"Alar chest" of phthisis, 194 
Albuminometer, 358 
Albuminuria of adolescence, 359 

anemic, 359 

boiling test for, 356 

cyclic, 359 

due to pus, 359 

to renal congestion, 359 

Esbach's test for, 358 

Heller's test for, 356 

in acute diffuse nephritis, 371 

indicative of renal disease, 359 

marked, or absent, in amyloid kid- 
ney, 334 

orthostatic, 359 

potassium ferrocyanide test for, 
357 

quantitative test for, 358 

transient, in chronic interstitial ne- 
phritis, 372 

trichloracetic acid test for, 357 
Albuminuric retinitis, 440 
Albumosuria, 360 

in Bradshawe's disease, 360 

in normal puerperium, 360 

microorganisms in, 360 

myelopathic, 360 
Alcohol poisoning, tremors in, 49 
Alcoholic epilepsy, 495 
Alcoholism, convulsions due to, 495 

facial expression in, 18 

hyperesthesia in chronic, 189 

morning vomiting in, 519 

symptoms of acute, 488 

tremor of tongue in, 123 
Alexia, 360 

Alkaptonuria, 136, 364, 335 
Allen's test in phthiriasis versicolor, 

137 
Allochiria in hysteria, 187 

in multiple sclerosis, 187 

in myelitis, 187 

in paralysis agitans, 187 

in tabes dorsalis, 187 
Amaurosis, 436 

in brain fever, 473 

uremic, 436, 509 
Amaurotic family idiocy, 70 
Amblyopia, 440 
Ameba coli, 320 
Amebic dysentery, 320 
Amphoric breathing in pneumothorax, 
221 
in small cavity, 221 



Amyloid disease of kidney, hyaline, 
fatty, and granular casts in 
urine in, 334 

of liver, 301 
jaundice in, 133 
Amyotrophic lateral sclerosis, hands in, 

44 
Analgesia in locomotor ataxia, 173 

in Morvan's disease, 44 
Anasarca, general. See General ana- 
sarca. 
Anchovy-sauce sputum, 530 
Anemia, 390 

albuminuria in, 359 

aplastic, 392 

blood changes in, 390 

Bothriocephalus latus a cause of, 327 

cerebral choked disk in, 510 

vertigo in, 483 

vomiting in profound, 510 
color index in, 390 
dropsy of feet and legs in, 163 
edema in, 163 
headache in, 482 
hiccough in, 508 
hyperesthesia in, 189 
in acute diffuse nephritis, 372 
in ankylostomum duodenale, 328, 391 
in atrophy of gastric tubules, 391 
in bleeding hemorrhoids, 390 
in cancer, 391 
in chronic indigestion, 390 

lead or arsenic poisoning, 391 
in convalescence from infectious dis- 
ease, 390 
in gastric ulcer, 391 
in hemorrhage, 391 
in malaria, 391 
in pyelitis, 342 
in renal disease, 391 
in sarcoma, 391 
in tape-worm, 391 
in tuberculosis, 391 
in uremic poisoning, 391 
nails in, 34 
of convalescence, dilatation of pupil 

in, 428 
oligochromemia in, 389 
oligocythemia in, 382 
pallor of conjunctiva in, 411 
papillitis in, 439 
pernicious, cardiac palpitation in, 392 

change in red blood corpuscles in, 
392 

chills followed by fever in, 459 

dyspnea in, 392 

fatty degeneration of heart in, 264 

hemoglobin estimate in, 389 

indicanuria in, 341 

jaundice in, 134 

marked pallor, without loss of 
flesh in, 392 



INDEX 



565 



Anemia, pernicious, oligocythemia in, 
382 
pulsating cervical vessels in, 203 
venous murmurs in, 392 
vertigo in, 392, 483 
purpuric eruptions in, 141 
secondary, 390 

blood in, 390, 391 
splenic, 310 

blood changes in, 310 
tongue in, 116 
Anemic heart murmur, 246 

necrosis, 264 
Anesthesia, 168 

bilateral, in chorea, 170 
in Friedreich's ataxia, 174 
in hemorrhage of cord, 174 
in hysteria, 172 
in injuries of cord, 173, 174 
in lesions of pons, 173 

»in locomotor ataxia, 173 
in meningitis, spinal, 173 
in myelitis, 173, 174 
in spinal disease, 173 
in syringomyelia, 175 

causes of, 168 

crossed, in lesions of one side of 
cord, 172 
of peduncle, 172 
of pons, 172 

differential diagnosis in facial, 185 

distribution of, in special nerve in- 
volvement, 184 

dolorosa in cancer of spine, 175 

gauntlet or stocking form of, 171 

in hysteria, 168 

in the spinal cord, 175 

neuritis as cause of, 180 

of body and legs in locomotor ataxia, 
173 

rof face, 185 
of Friedreich's ataxia, 174 
of myelitis, 173, 174 
of toxic peripheral neuritis, 181 
patches of, in syringomyelia, 175 
reflexes preserved in cerebral, 171 
signs of, due to neuritis, 180 
unilateral, 171 
varieties of, 169 
zones of, 175, 177-180 
Aneurysm, aortic, blood-streaked spu- 
tum due to leakage from aorta 
in, 529 
bruit in, 251 

bulging of chest in, 196, 253 
hemopt}rsis in, 529 
pain in, 254, 529, 540 
appearance of hands in, 34 
brassy cough due to pressure on 

larynx bv, 253, 527 
bruit in, 251, 253 
dyspnea or dysphagia in, 125, 253 



Aneurysm, edema of upper extremities 
in, 164 
enlarged cervical vessels in, 202 
hemorrhagic pleural effusion in, 238 
hoarseness of voice due to pressure 
on recurrent larvngeal nerve bv, 
253, 557 
intracranial, headache due to, 482 
laryngeal spasm due to pressure on 
recurrent laryngeal nerve bv, 242, 
252 
loss of pulsation in peripheral ves- 
sels in, 255 
of abdominal aorta, 305 
pain in abdominal, 540, 547 
pressure on bile duct causing jaun- 
dice in, 131 
sweating of side of head in, 161 
symptoms of, 251 
syphilis in, 251 

thoracic diagnosis of, from medias- 
tinal growths, 243 
pain in, 243 
tracheal tugging in, 254 
Angina pectoris, causes of, 268 
pain in, 539, 540 
symptoms of, 540 
Angioneurotic edema, evelids in, 143, 
164 
hands in, 39 
skin in, 143 
Ankle clonus, how best elicited, 553 
in amyotrophic lateral sclerosis, 555 
in ataxic paraplegia, 66 
in disseminated sclerosis, 555 
in hysteria, 555 
in lateral sclerosis, 555 
Ankylostomiasis, eosinophilia in, 396 
Ankylostomum duodenale, 327 

anemia due to, 391 
Annulus migrans, 120 

senilis, 412 
Anthrax maligna, anthrax bacilli in, 
156 
fever in, 156 
symptoms of, 156 
simplex. See Carbuncle. 
Antidiphtheritic serum, roseola due to 

injection of, 148 
Anus, fissure of, diarrhea in, 318 
Aorta, aneurysm of abdominal, 305 
of descending, symptoms of, 254 
of greater curvature of ascending, 

symptoms of, 253 
of transverse portion of arch of, 
symptoms of, 253 
Aortic aneurysm, bruit in, 251 

diagnosis of, by fluoroscope, 255 
pulse in, 251 
regurgitation, 250 
"ox-heart" of, 250 
pulse in, 273 



566 



INDEX 



Aortic regurgitation, Quincke's sign of, 
259 
"water-hammer" pulse in, 250 
stenosis, 250 
pulse in, 273 
reduplication of heart sounds in, 

246 
symptoms of, 259 
valvular disease, 250 
Aortitis, acute, causes of, 540 

pain in, 539 
Apex beat, 205 
Aphasia, 559 

due to hematoma near island of 
Reil, 108 
to hemorrhage into island of Reil, 
108 
Aphemia, 560 

Aphonia due to pressure in aortic an- 
eurysm, 252 
in hysteria, 557 
Aphthongia, spasm of tongue in, 123 
Aplastic anemia, 392 
Apoplexy, cause of, 267 

Cheyne-Stokes breathing in, 201, 488 

coma in, 488 

conjugate lateral paralysis of ocular 

muscles in, 423 
contractions following, 45 
diagnosis between coma of, and alco- 
holism, 488 
epilepsy associated with, 493 
ingravescent, 105 
knee-jerk decreased after shock, 553 

exaggerated after shock, 554 
paralytic chorea following, 47 
passage of urine in, 332 
peptonuria in, 360 
skin reflexes lost when deep reflexes 

are exaggerated, 555 
vertigo before, 483 
Appendicitis, fever in, 289 
leukocytosis in, 395 
pain in, 289, 543, 545 
symptoms of, 289 

in groin, 313 
vomiting in, 516 
Apraxia, 260 
Arcus senilis, 264, 412 
Argyll-Robertson pupil, 60, 427 

not present in ataxic paraplegia, 

66 
in Friedreich's ataxia, 63 
in true ataxia, 427 
present in diabetes mellitus rarely, 
60, 427 
Argyria, 136, 137 

Arhythmia in cardiac dilatation, 263 
Arms, spastic rigidity of, sign of trem- 
ors, of 46 
tumors of, 49 
Arsenical neuritis, 50 



Arterial disease, ophthalmoscopic evi- 
dence of, 441 
sclerosis, heart sounds in, 245 
tension, 267 

causes of, 267, 269 
estimation of, 270 
in acute diffuse nephritis, 372 
Arteritis, syphilitic, 474 

facial paralysis in, 20 
Artery of cerebral hemorrhage, 105 
Arthralgic form of gonorrheal arthri- 
tis, 89 
Arthritis deformans, fingers in, 36, 37 
formation of osteophytes in, 90 
hand in, 46 

Heberden's nodes in, 37 
joints in, 89, 90 
knee-jerk increased in, 554 
seal-fin hand of, 37 
gonorrheal, 89 
in acute osteomyelitis, 91 
multiple, in dengue, 92 
of cerebrospinal meningitis, 91 
septic, hands in, 38 
joints in, 91 
Arthropathies, 89 
Ascarides, enlargement of gall-bladder 

due to, 292 
Ascaris lumbricoides, 327 
Ascites, apex beat raised in, 206, 284 
caput Medusse in hepatic cirrhosis 

causing, 285 
diagnosis of, 283 
examination of withdrawn fluid in, 

284 
rapid respiration in, 202 
skin of abdomen in, 202 
Astasia abasia, 68 
Astereognosis, 166 
Asthenic bulbar paralysis, 26 
Asthma, catarrhal pneumonia follow- 
ing, 241 
character of rales in, 241 
due to cardiac lesions, 241 
to gastric disorders, 241 
to reflex nasal irritation, 241 
to renal disease, 241 
erect position in, 241 
expiration prolonged in, 201, 241 
physical signs and symptoms of, 241 
rapid respiration in, 200 
sputum of, Charcot-Leyden crystals 
in, 241, 531 
Curschmann's spirals in, 241 
pearls of mucus in, 530 
Asymmetry, facial, 16 
Asynchronism of ventricles, reduplica- 
tion of first sound of heart due to, 
246 
Ataxia, differential diagnosis of, 63 
Friedreich's. See Friedreich's ataxia, 
hereditary cerebellar, 64 



INDEX 



567 



Ataxia, hereditary spinal. See Fried- 
reich's ataxia. 
Locomotor. See Locomotor ataxia. 
Ataxic paraplegia, 66, 83 
Atheroma, headache in, 471 

in chronic interstitial nephritis, 372 
vertigo in, 483 
Athetosis, 52 

reflexes increased in, 55.5 
Atrophy, acute yellow, of the liver, 
coma in, 487 
convulsions in, 504 
hematemesis in, 518 
jaundice in, 134 
vomiting in, 522 
bilateral, of tongue, causes of, 120 
faciohumeroscapular type of, 14 
idiopathic muscular, ptosis in, 24 
in gastric dilatation, 298 
of gastric tubules, anemia in, 391 
of nails, 35 
optic, 440 
progressive muscular, 42 

Aran-Duchenne type of, 89 
clawhand in, 42 
condition of reflexes in, 555 
fibrillary twitch in, 51 
leg symptoms of, 74, 89 

type of, 75, 89 
peroneal leg type of, 75, 89 
sweating of hand in, 36 
unilateral, of tongue in chronic lead 
poisoning, 120 
Aura, 491 
Auscultation of heart and vessels, 244 

of respiratory apparatus, 219 
Auto-intoxication, headache in, 470 
poisons causing, 470 
S3nmptoms of, 470 



Babinski's reflex, 555 
Baccelli's sign, 225 
Bacilli, anthrax, 156 
in preputial smegma, 353 
in stools in cholera, 317 
in tuberculous pyelitis, 342 
of Eberth, in stools of typhoid fever, 

449, 451 
tubercle, in sputum, examining for, 
534-536 
in urine, 353 
Bacillus typhosus, cause of empyema, 

239 
Banti's disease, 310 

symptoms of, 310, 311 
Barrel-shaped chest in emphysema, 

195, 240 
Basedow's disease, tremor of hand in, 
50 



Bed-sores in acute transverse myelitis, 
77, 158 
in hemiplegia, 158 

in hemorrhage into spinal cord, 75 
in typhoid fever, 158 
Bence-Jones' albumin in urine in bone 

tumor, 355 
Bergeron's chorea, 48 
Beriberi, general anasarca in, 163 
Biceps, tendon reflex, how developed, 

58 
Bilateral anesthesia, 172 
facial paralysis, 25 
ptosis, 24 
wrist-drop, 46 
Bile ducts, obstruction of, 292, 293 

in urine, test for, 341, 365 
Bilious remittent fever. See Malaria, 

remittent. 
Biliousness, tongue in, 114 
Bismuth, odor of breath after admin- 
istration of, 3 
Black vomit in yellow fever, 460 
Bladder, 329 

causes of incontinence of urine in, 
332 
of retention of urine in, 330 
character of blood in urine from. 335 
nervous, 333 
paralysis of, 330 
sensory disorders of, 332 
stone in, 332 

symptoms of diseases of, 329 
of inflammation of, 332 
of locomotor ataxia, 331 
of myelitis, 77, 330 
of paretic dementia, 331 
of tabes, 331 
tumors of, obstructing urinary flow, 
332 
Blepharofacial spasm, 27 
Blindness, causes of, 429, 436 
Blood, 374 

casts in urine, 346 

changes in, causing albuminuria, 359 

in infectious diseases, 390 
circulation of, 266 
color index of, 389 
diagnostic value of, in appendicitis, 

395 
estimation of hemoglobin in, by 
Dare's hemoglobinometer, 387 
by hemoglobinometer of v. 

Fleischl, 385 
by specific gravity method, 388 
by Tallquist's method, 389 
Filaria sanguinis hominis in, 403 
in sputum, 529 
in stools, 320, 322, 323, 515 
in dysentery, 319, 320 
in enterocolitis, 318 
in urine, 335 



568 



INDEX 



Blood in urine, guaiacum test for, 360 
Heller's test for, 360 
in severe renal disease, 548 
in vomitus, 517, 518 
method of examining, 375 

of staining with Ehrlich's triple 
stain, 384 
microscopic examination of, 375 
normal constitution of, 374 
opsonic index, method of testing, 408 
parasites of, 396 

red corpuscles of, changes in, in ane- 
mia, 390 
coloring matter of, decreased in 

anemia, 389 
decreased in myelogenous leu- 
kemia, 394 
in anemia of all types, 382 
estimation of, by hematocy- 
tometer, 376 
with hematocrit, 380 
extraordinary decrease of, in 

pernicious anemia, 392 
increase in, causes of, 382 
macrocytes, 385 
megaloblasts, 392 
megalocytes, 385 
microcytes, 385 
normoblasts, 385 
nucleated, 385 
poikilocytes, 385 
proportion of, to white, 374 
shadow corpuscles, 385 
significance of variation in num- 
ber of, 382 
varieties of, 374 
streams of retinal, influence of arte- 
rial pressure on, 441 
sugar in, 408 

Williamson's test for, 408 
trypanosoma in, 405 
white corpuscles of, ameboid move- 
ments of, 383 
basophiles, 383 
eosinophiles, 383 
estimation of, with hematocy- 

tometer, 379 
increase of, 383, 394 
lymphocytes, 383 

increased in lymphatic leu- 
kemia, 395 
mononuclear leukocvtes, 383 
multinuclear leukocytes, 383 
neutrophiles, 383 
polymorphous leukocytes, 383 
polynuclear leukocytes, 383 
proportion of, to red, 374 
Toison's solution for counting, 
379 
Widal's test of, in typhoid fever, 
406 
Bloodvessels and pulse, 265 



Blue line on gums in lead poisoning, 60, 

124 
Boiling test for albumin in urine, 355 
Boils in diabetes mellitus, 156 
in paraffin-workers, 156 
in tar-workers, 156 
Bone tumors, Bence-Jones' albumin in 

urine in, 355 
Bothriocephalus latus, 327 
Bowels, cancer of, 306 

constipated, in jaundice, 131 
sloughs of, in intussusception, 324 
Brachial monoplegia, 52 
apparent, 55 
bilateral, 55 
cortical lesions in, 53 
due to cortical lesions, 52 
to crutch paralysis, 55 
to fracture or dislocation of the 

head of humerus, 54 
to growth in neck or axilla, 55 
to hysteria, 53 
to injury of brachial plexus or 

important branches, 54 
to lead poisoning, 55 
to locomotor ataxia, 54 
to primary brachial neuritis, 54 
Erb's paralysis, 55 
Klumpke's paralysis, 55 
paralysis of special muscles in, 55 
signal symptoms of cortical, 52 
paresthesia, 56 
Bradshawe's disease, albumosuria in, 

360 
Bradycardia, 263, 276 
in jaundice, 263 
in some infectious diseases, 263 
Brain, areas of, 99 

tumors of, anesthesia in, 170 
Cheyne-Stokes breathing in, 201 
convulsions in, 473 
diagnosis of, 474 

differential, between chronic ne- 
phritis and, 474 
headache in, 472 
hyperesthesia in, 189 
papillitis of optic nerve in, 439, 472 
paralysis in, 473 
paresthesia m, 186 
slow breathing in, 474 

pulse in, 474 
vomiting in, 472 
Bramwell's method of staining and 

mounting casts in urine, 349 
Brandberg's method of determining 

the cause of pleural effusion, 237 
Breakbone fever, 147. See Dengue. 
Breast, pigeon, 198 

Breath after the administration of bis- 
muth, 3 
in bronchiectasis, 3, 232 
in chronic atrophic nasal catarrh, 3 



INDEX 



569 



Breath in diabetes mellitus, 3 
in diphtheria, 3 

in empyema opening into bronchus, 3 
in fever, 3 

in gangrenous stomatitis, 3 
in gastric disorders, 3 
in heart disease, 258 
in ozena, 3 

in pulmonary gangrene, 3, 232 
in tonsillitis, 3 
in uremia, 3 
Breathing, abdominal, 202 
amphoric, 221 
blowing, 220 
bronchial, 219, 220 
bronchovesicular, 220 
cavernous, 221 
cog-wheel, 220 
costal, 202 
irregular, 220 
puerile, 220 
tubular, 219, 220 
vesicular, 219, 220 
wavy, 203 
Bright's disease. See also Kidneys and 
Nephritis. 

complications of, 373 

estimation of urea in, 369 

obstinate cough in, 526 

retinal hemorrhage in, 440 

retinitis in, 441 

roseola in, 148, 149 

secondary diphtheritic dysentery 
in, 320 

sputum in, 530 
Broadbent's sign of adherent pericar- 
dium, 204 
Bromidrosis, cold, clammy hands in, 36 

in hysteria, 161 
Bronchial breathing, 219, 220 

due to compression of lungs over 
pleural effusion, 220 

in catarrhal pneumonia, 220 

in cavity, 220 

in consolidation, 220 
Bronchiectasis, fetid breath of, 3, 232 
purulent sputum in, 530 
sacculated morning cough in, 526 
Bronchitis, acute, sputum in later 

stages of, 528 
bronchorrhea in, 240 
Charcot-Leyden crystals in, 531 
chronic, in chronic interstitial ne- 
phritis, 373 
fever in, 465 
fibrinous, small casts of bronchioles 

coughed up in, 531 
hard, dry cough in, 239, 525 
moderate, early in typhoid fever, 451 
physical signs of, 239 
purulent, crystals of margaric acid in 

sputum of, 532, 533 



Bronchitis, putrid, 240 

Dittrich's plugs in sputum of, 240 
rales, 240 

bubbling, 222 
rapidity of respiration in severe, 200 
Bronchophony in pleural effusions, 226 

in tuberculosis of lungs, 230 
Bronchovesicular breathing, 220 
Brow ague in malaria, 482, 537 
"Bruit" in aortic aneurysm, 251, 253 
Bullae due to antipyrine or iodine, 157 
to pemphigus, 157 
to trophic lesions in diseases of 
central nervous system, 157 
Burns, hemoglobinuria after severe, 

340 
Bursal gonorrheal arthritis, 89 



Cachexia, anasarca in cancerous, 163 
Calculi, fecal, 324 
Calculus. See also Stone, 
pancreatic, pain in, 544 
renal, pain in, 548 

vomiting in, 522, 548 
salivary, 126 

vesical, symptoms of, 332, 548 
Caput coli, diseases of, 313 

Medusas, 285 
Carbol-fuchsin stain for tubercle bacilli, 

534 
Carbuncle, 156 

Carcinoma, face in, expression of, 11 
pallor of, 136 
esophageal, brassy cough due to 
pressure on larynx by, 527 
stricture due to, 1 25 
gastric anemia in, 290, 391 
character of vomiting in, 517 
coffee-ground vomit in, 290, 517 
fever in, 459 
indicanuria in, 341 
most frequent at pylorus, 290 
hemorrhagic effusion in pleura in, 238 
melanotic, black urine in, 335 
of bowel, 306 
of caput coli, 313 
of gall-bladder, 292 
of liver, indicanuria in, 341 
of pancreas, diabetes mellitus in, 
294 
jaundice in, 133, 294 
of pylorus, diagnosis of, 290 

between gastric ulcer and, 291 
dilatation of stomach due to. 290 
lactic acid in stomach in, 299 
symptoms of, 290 
renal hematuria in, 337 
retraction of abdominal wall in, 281 
skin in, 136 



570 



INDEX 



Carcinoma, visceral^peptonuria in, 360 
Cardiac crises, 264 
dilatation, 259 

diseases in children, pain in, 6 
dulness, alterations in, due to valvu- 
lar lesion, 218 
increase of, due to hypertrophy or 
dilatation of heart, 214 
due to pericardial effusion, 215 
normal extent of, 213 
feebleness, 264 
neurosis, 263 
triangles, 213 
Cardiopulmonary murmur, 246 
Caries of bones of skull, headache in, 
482 
of cervical vertebrae, head in, 30 
of teeth in pregnancy and diabetes 

mellitus, 124 
of vertebrae, paraplegia due to, 69 
spinal, symptoms of, 541 
Carphologia, 36, 51 
Carpopedal spasm, in rickety, hydro- 

cephaloid children, 46 
Casts, Bram well's method of mounting 
and staining, 349 
centrifuge in examining, 345 
composition of, 344 
Farrant's solution for staining, 350 
fatty, 347 
hyaline, 347 
of blood cells, 346 
of bronchioles found in sputum, 531 
of epithelial cells, 345 
of granular matter, 346 
of micrococci, 346 
of pus cells, 346 

resemblance to cylindroids to, 348 
Catalepsy, 14 
Cataract, congenital, nystagmus in, 425 

result of diabetes mellitus, 441 
Catarrh, acute gastric, symptoms of, 
518 
tongue in, 115, 518 
vomiting in, 518 
rectal, symptoms of, 319, 320 
chronic gastric, morning vomiting of 
drunkards in, 519 
vomiting due to excessive tea- 
drinking in, 519 
gastro-intestinal, fever in mild, in 
children, 446 
frog-belly in children with, 281 
uric acid, excess in urine of, 351 
laryngeal spasm, due to, 242 
nasal, headache due to, 482 

chronic, odor of breath in, 3 
of middle ear in syphilis, 124 
persistence of fever in measles due 
to bronchial or gastro-intestinal, 
454 
respiratory cough in, 527 



Catarrhal fever. See Influenza, 
jaundice, 131 

pneumonia. See Pneumonia, catar- 
rhal. 
Cavernous breathing, 221 

sinus, thrombosis of, 480 
Centrifuge, 380 

in examination of blood, 380 

of urine, 345 
test for albumin with, 358 
Cephalalgia. See Headache. 
Cephalic tetanus, 29 
Cerebellar ataxia, hereditary, 64 
disease, gait in, 67 

vomit in, 523 
hemorrhage, 108 
titubation, 67 
Cerebral abscess, coma in, 489 
pain in, 539 
papillitis in, 439 
effusion, 31 
embolism of brachial monoplegia in, 

52 
hemiplegia in, 108 
hemorrhage, artery of, 105 

ptosis from, 22 
lesions, increased urinary flow in, 334 
palsy of children, 44 
athetosis in, 52 

epileptiform convulsions in, 45 
flexion of hands in, 44 
gait in, 66 

intention tremor in, 45 
knee-jerk in, 554 
softening, coma of, 488 

symptoms of, 488 
spastic paraplegia, 69 
syphilis, coma in, 490 

hemiplegia in, 109 
thrombosis, edema in, 164 

hemiplegia in, 108 
tumor, pain in, 539 

spastic hemiplegia in, 109 
Cerebrospinal fever, Cheyne-Stokes re- 
spiration in, 201 
fluid, trypanosoma in, causing sleep- 
ing sickness, 405 
meningitis, 461 

character of fever in, 461 
convulsions in, 461 
diagnosis between croupous pneu- 
monia, otitis media, tubercu- 
lous infection, and, 462 
lumbar puncture in, 462 
peptonuria in, 361 
epidemic, coma in, 490 
headache in, 461 
herpes labialis in, 155 
hyperesthesia in, 188 
joints in, 89, 91 
petechias in, 142 
retraction of head in, 30 



INDEX 



571 



Cerebrospinal meningitis, rigidity of 
back of neck in, 461 
vomiting in, 461 
sclerosis, multiple, 71 
Cestodes, 326 
Chancre of tongue, 118 
Charcot-Leyden crystals in acute bron- 
chitis, 531 
in asthmatic attacks, 241, 531 
in chronic croupous pneumonia, 

531 
in pulmonary tuberculosis, 531 
Charcot's fever, 132, 457 
Cheek, swelling of, in noma, 126 
in peliosis rheumatica, 126 
in salivary calculus, 126 
in Schonlein's disease, 126 
in stomatitis, 126 
Chemical tests of urine, 355 
Chest, auscultation of, 219 

barrel-shaped, of emphysema, 195 
beaded ribs of, in rickets, 198, 199 
bulging of, causes of, 195 

of sternum in pigeon breast , 1 98 
expansion, 203 
friction sounds in, 223 
Harrison's grooves in, 198 
inspection of abnormal, 194 

of normal, 191 
localized bulging of, 195, 202 
pain in, in children, 11 
palpation of, 204 
percussion of, 207 
phthisical or alar, 194 
resonance of, 208 
shrinking of, 199 
tumors of, 242 

variation in shape of, in health, 194 
wall, pulsations on, causes of, 2C3 
Cheyne-Stokes respiration, causes of, 
201 
prognostic value of, 201 
pupillary reaction associated with. 
429 
Chickenpox, eruption in, 154 
fever in, 455 

disparity between height of, and 
degree of illness in, 455 
Chill in acute pleurisy, 232 
in croupous pneumonia, 464 
in dysentery, 319 
in intermittent malarial fever, 455 
in pernicious anemia, 459 
in pjrelitis, 342, 459 
in septic poisoning, 459 
Chills, 442 
Chilly sensations and nausea in acute 

diffuse nephritis, 371 
Chin jerk, how elicited, 552 

position of, in wryneck, 29 
Chlorides in urine, 370 
tests for, 370 



Chlorosis, appetite in, 393 
constipation in, 393 
disorders of menstruation in, 393 
dyspnea in, 393 
fever in, 393 

greenish-yellow color in, 136 
hemoglobin decreased in, 392 
humming-top murmur in jugular 

vein in, 393 
irregular heart in, 393 
pallor of, 10, 138 
poikilocvtosis in, 392 
Choked disk, 439 

in cerebellar tumor, 439, 510 
in cerebral anemia, 510 
tumor, 439, 510 
Cholangitis, catarrhal or suppurative, 
fever in, 457 
gallstone colic in, 457 
jaundice in, 457 
leukocytosis in, 457 
Cholecystitis, acute, pain in, 543 
Cholelithiasis, 544 

Cholera Asiatica, comma bacillus in, 
317 
diagnosis of, 316, 317 
Hippocratic face in impending 

death in, 14 
indicanuria in, 341 
roseola in, 148, 149 
skin in, 161 

subnormal temperature in, 467 
systemic infection in, 317 
temperature in, 316 
vomiting in, 516 
infantum, fever in, 316 
odor of stools in, 322 
Cheyne-Stokes respiration in, 316 
cold skin and high rectal tempera- 
ture in, 316 
diarrhea in, 316 
disparity between axillary and 

rectal temperatures in, 316 
sinking in of fontanelles in, 32 
subnormal temperature in, 467 
symptoms of, 316 
vomiting in, 517 
morbus, subnormal temperature in, 
467 
symptoms of, 316 
nostras. See Cholera morbus. 
Chorea, anemic murmurs in children in, 
246 
anesthesia in, 170 
Bergeron's, 48 
character of spasms in, 505 
diagnosis of, 505 
electric, 48, 506 
expression in, 14 
facial spasm in, 27 
habit, 47 
heart disease in, 246 



572 



INDEX 



Chorea, hemianesthesia in, 170 
hereditary, 48 
Huntingdon's, 48, 506 
hysterical, 48 
incoherent speech in, 559 
insaniens, 505 
loss of knee-jerk in, 553 
major, 506 
maniacal, 47 

minor, movements in, 47, 505 
nodding spasm in, 28, 29 
paralytic, 47 

posthemiplegic lesion of, 108 
senile, 47 

spasm of face in, 26 
of tongue in, 123 
Choroid, tubercle of, 477 
Chromophytosis, skin in, 137 
Chvostek's symptom of tetany, 504 
Chyluria, caused by Filaria sanguinis 
hominis, 339, 341, 405 
test for, 341 
Circulatory changes, albuminuria due 

to, 359 
Cirrhosis, hepatic ascites in, 163, 284, 
302 
caput Medusae in, 285 
disorders of digestion in, 302 
enlargement of spleen in, 310 
hematemesis in, 302, 518 
jaundice in, 132 
symptoms due to, 302 
uric acid in urine of, 351 
Clawfoot, 75 

in Friedreich's ataxia, 75 
Clawhand, 40 

Clothing, diagnostic significance of, 2 
Clubbed fingers, 34, 258 
Coffee-ground vomit in gastric cancer, 
517 
in locomotor ataxia, 517 
in phosphorus poisoning, 521 
Cog-wheel breathing, 220 
Coin percussion in pleural effusion with 

pneumothorax, 235 
Cold abscess of mediastinum, 243 
Colic, abdominal, 543 
in children, 7 
due to Strongylus gigas, 338 
gallstone, in catarrhal cholangitis, 

292 457 
hepatic, 131, 543 
lead, pain in, 547 
renal, pain in, 547 

diagnosis of, 547, 548 
retraction of abdominal wall in re- 
nal, hepatic, and lead, 281 
ureteral, 336 
Collapse, profuse sweating a sign of, 161 
of lung, tympanitic percussion sound 
in, 211, 212 
"Collar of brawn" in scarlet fever, 453 



Colon bacillus as a cause of empyema, 

239 
Coma, ability to protrude tongue in, 
when other orders fail to gain re- 
sponse, 121 

causes of, 484 

following pernicious malarial fever, 
487 
position in, 4 

in acute alcoholic poisoning, 484 

differential diagnosis of, 484, 
485 
yellow atrophy of liver, 486 

in Addison's disease, 490 

in apoplexy, 488 

in cannabis indica poisoning, 485 

in cerebral abscess, 489 
disease, 4 
softening, 488 
syphilis, 490 

in chloral poisoning, 486 

in chronic parenchymatous nephritis, 
372 

in cirrhosis of liver, 302 

in diabetes, 373, 486 

in epidemic cerebrospinal menin- 
gitis, 490 

in epilepsy, 490 

in general paralysis, 490 

in heart failure, 490 

in heat-stroke, 490 

in multiple sclerosis, 490 

in opium poisoning, 485 

in pernicious malarial infection, 487 

in petit mal, 490 

in purulent leptomeningitis, 489 

in Raynaud's disease, 489 

in renal disease, 4, 5 

in subdural hemorrhage, 489 

in thrombosis of brain sinuses, 489 

in typhoid fever, 486 

in uremia, 486 

rapidity of respiration in diabetic or 
uremic, 201, 487 

slowness of breathing in uremic or 
diabetic, 201, 487 

vigil, 487 
Concomitant squint, 414 
Congenital asymmetry of face, 16 

cardiac disease, diagnosis of, 255 

cataract, nystagmus in, 425 

lymphangioma, tongue in, 120 

malformations of heart, 255 
rules for diagnosis of, 255 

ptosis with facial paralysis, 22 
Congestion, hepatic tenderness in, 302 

pulmonary, 232 

renal, albuminuria in, 359 
blood casts in, 346 
Consensual pupillary reflex to light, 426 
Constipation, causes of, 314 

in chlorosis, 393 



INDEX 



573 



(Constipation in chronic lead poisoning, 
315 

in diabetes insipidus, 314 

mellitus, 314 
in hepatic disease, 314 
in intestinal obstruction, 315, 509, 

511, 514 
in jaundice, 314 
in pelvic disorders, 315 
in phosphorus poisoning, 314 
in reflex irritation, 315 
indicanuria in, 341 
Continued fever. See Malaria, remit- 
tent. 
Contraction of pupil of eye, 427 
Contractures in hysteria, 45, 73 
Convulsions or general spasms, 491 

in acute articular rheumatism 

with hyperpyrexia, 466 
in Addison's disease, 503 
in anterior poliomyelitis, 84 
in brain tumor, 473 
in cerebrospinal meningitis, 461 
in uremia, 496, 500 
clonic, at onset of apoplexy, 493 
in acute alcoholism, 495 
in chronic lead poisoning, 496 
in epilepsy, 491 
in general paresis, 63 
in hysteria, 498 

in irrigation of pleural cavity, 503 
in Jacksonian epilepsy, 492 
in malaria, 497 
in malingerers, 502 
in multiple sclerosis, 503 
in posthemiplegic epilepsy, 493 
in puerperal eclampsia, 501 
in syncope, 502 
in syphilitic epilepsy, 494 
epileptiform, in cerebral palsy of 

children, 45 
erotic, in phosphorus poisoning, 521 
of infants in meningitis, 502 
in pseudomeningitis, 503 
in reflex irritation, 502 
salaam, 506 

tetanic, in acute yellow atrophy of 
liver, 504 
in hematoma of dura mater, 504 
in strychnine poisoning, 503 
in tetanus, 503 
in tetany, 504 
Convulsive tic, 48 

facial spasm in, 27 
Coprolalia, 27, 48 
Coproliths, 324 

Corneal ulceration in scrofulosis, 441 
Corpuscles of Ehrlich, 392 
Corrigan's pulse, 250, 259, 273 
Coryza, action of child toward breast 
in, 7 
in influenza, 464 



Cough and expectoration, 525 
causes of night, 527 
chronic loose, in empyema, rupturing 
into bronchus, 526 
in pulmonary abscess, 526 
in sacculated bronchiectasis, 526 
in tuberculosis with cavity, 526 
dry and hacking, in phthisis pulmo- 
nalis, acute bronchitis, and pneu- 
monia before exudation, 525 
due to change of position in pleurisy 

with effusion, 527 
during aspiration of fluid in pleurisy, 

527 
followed by cry in pneumonia of 

pleurisy, in children, 7 
hard and drv, in acute bronchitis 239, 

525 
in acute laryngitis, 527 
in aneurysm of transverse arch of 

aorta. 253 
in false croup, 525, 527 
in laryngeal phthisis, 527 
in whooping-cough, 52.") 
larvngeal, due to irritant, dust or 
vapors, 525, 527 
to mediastinal tumors, 527 
to pressure by aneurysm, 527 

bv carcinoma of esophagus, 
"527 
nervous or reflex, 526 
obstinate, in Bright's disease, 526 
produced by enlarged tonsils, en- 
larged uvula, hypertrophy of mu- 
cous membrane of the nose, etc., 
527, 528 
significance of cessation of, in ad- 
vanced phthisis, bronchorrhea of 
old and severe pneumonia, 528 
smothered or suppressed, in pleuro- 

pulmonarv inflammation, 526 
value of loose, 526 
varieties of, 525 
Courvoisier's law, 293 
Coxalgia, pain in, 6, 541 
Cracked-pot sound, 211, 212 
Craniotabes, 31 
Creatin in urine, 351 
Creatinin in urine, 351 
Cremasteric reflex, 98, 552 
Crepitant rales, 222 
Cretinism, facial expression in, 15 

shape of head in, 31 
Cretinoid edema, 144 
Crisis, apparent, in relapsing fever, 453 
fever in erysipelas ending by either 

lysis or, 455 
gastric, in locomotor ataxia, 60, 517 
in croupous pneumonia, 464 
in typhus fever, 452 
intestinal, 318 
subnormal temperature at, 467 



574 



INDEX 



Crisis with fading of eruption in measles, 

454 
Croup, spasmodic, cough in, 525, 527 
inspirations prolonged in, 201 
laryngeal spasm in, 242 
Croupous pneumonia. See Pneumonia, 

croupous. 
Crutch palsy, 46 
Crying in children, 7 
Cryoscopy in pleural effusion, 238 
Crystals, ammonium urate, 352 

amorphous phosphates, 352 

blood, of Teichmann, 340 

Charcot-Leyden, 241, 531 

creatin, 351 

creatinin, 351 

hemin, 524 

oxalate of lime, 350 

triple phosphates, 350, 352 

urates, 350, 352 

uric acid, 350 
Curschmann's spirals in asthmatic at- 
tacks, 241, 530 
in croupous pneumonia, 530 
in pulmonary tuberculosis, 530 
Curvature of spine, bulging of chest in, 

198 
Cyanosis, causes of, 138, 139 

due to drugs, 139 

in acute articular rheumatism with 
hyperpyrexia, 466 
miliary tuberculosis, 464 

in cardiac dyspnea, 10 

in laryngeal obstruction, 139 

in newborn, 138 

in pulmonary diseases, 139 

in serious cardiac disease, 139 
Cyclic albuminuria, 359 
Cyclical vomiting, 520 
Cylindroids, varieties of, 348 
Cyst, echinococcus, of kidney, 307 

hematuria in renal, 337 

hydatid, of liver, 304 

of kidney, 307 

of mesentery, 309 

of pancreas, 304 

ovarian, diagnosis of, 281 
Cystic degeneration of kidney, 307 
Cystitis, acute, hematuria due to, 338 

chronic, triple phosphates in urine 
in, 350, 352 

pain in, 550 

in urethra in, 331 

purulent, septic fever in, 329 

tenesmus in, 331 
Cytodiagnosis in serous pleural effu- 
sion, 236 



Dactylitis, 35 

syphilitica in infants, 35 
Dare's hemoglobinometer, 387 



Deafness, chronic, position of head in, 

30 
Deformity of feet and legs, 88 

in acute cerebral paralysis of 
infancy, 75 
Degenerative myocarditis, 264 
Delirium, in acute articular rheuma- 
tism with hyperpyrexia, 466 
yellow atrophy of liver, 487 
in croupous pneumonia, 227 
in thrombosis of cerebral sinuses, 480 
incoherent speech in, 559 
low, muttering, in typhoid fever, 13, 

451 
mild, in mitral regurgitation, 482 
wild, in phosphorus poisoning and 
in some cases of uremia, 521 
Dementia, paretic, Argyll-Robertson 
pupil in, 427 
diplopia in, 413 
gangrene in, 157 
hemiplegia in, 109 
hemorrhage into skin in, 142 
hesitating, halting speech in, 559 
knee-jerk in, 554 
localized sweating in, 161 
optic atrophy in, 440 
perforating ulcer of foot in, 158 
tache cerebrale in, 144 
tremor of tongue in, 559 
Dengue, 460 

differential diagnosis of, 460, 461 
erythema in, 147 
fever in, 460 
hematemesis in, 518 
jaundice in, 134 
joint involvements in, 92 
pain in, 551 
Dentition, fever in, 446 
Dermatitis, acute exfoliating, 148 
Diabete bronze, 133 
Diabetes insipidus, constipation in, 314 
increase of urine in, 334 
loss of knee-jerk in, 553 
urine of, 373 
mellitus, acetonuria in, 364 

Argyll-Robertson pupil in, 60, 427 

boils in, 156, 364 

breath in, 3 

caries of teeth in, 124 

cataract in, 411, 441 

Cheyne-Stokes respiration in, 201 

coma in, 373, 486 

diagnosis of, 487 
constipation in, 314 
development of, in carcinoma of 

pancreas, 294 
dry, harsh skin in, 161, 162, 373 
erythema in, 373 
fermentation of urine in, due to 

Saccharomyces albicans, 355 
furunculosis in, 373 



INDEX 



:>7r, 






Diabetes mellitus, gangrene in, 158, 
373 

of toes in, 95 

headache rarely in, 472 

jaundice in, 133 

knee-jerk lost in advanced, 553 

ocular palsy in, 421 

paraplegia rare in, 85 

perforating ulcer of foot in. 95 

polydipsia in, 363 

polyphagia in, 363 

prognosis of, 363 

pruritus in, 190, 373 

retinitis in, 441 

roseola in, caused by urine. 150 

rosette crystals of uric acid in, 351 

urine in, 331, 373 
color of, 373 
increase of, 334 
odor of, 335 
specific gravity of, 373 

vomiting rare in, 509 

wasting in, 364 
of hands in, 40 

white spots on trousers in, 2 
Diarrhea, causes of. 315 
colliquative, in uremia. 509 
decrease of urine due to, 334 
dissecting room, 321 
due to heat prostration. 317 
fatty, due to cod-liver oil. 321 
to disease of pancreas, 321 

in jaundice, 321 
in abdominal pain, 6 
in acute antimony poisoning. 317 
in arsenic poisoning. 317 
in cholera Asiatica, 316. 317 
infantum, 316 
morbus, 316 
in dysentery. 319 
in enterocolitis, 318 
in fissure of anus, 318 
in hysteria. 321 
in influenza, 464 
in leukemia. 395 
in locomotor ataxia. 318 
in malignant ulceration. 320 
in proctitis. 319 

in pulmonarv gangrene or tuberculo- 
sis, 321 
in renal disease. 317 
in septicemia, 321 
in syphilitic ulceration, 321 
in tuberculosis, 319 
lienteric, 318 

may be caused by purgatives. 6 
nervous, 317 
pain in, 6 
paroxysmal, seromucous or bloody, 

in exophthalmic goitre, 321 
summer, retraction of bell v- wall in, 

281 



Diazo-reaction, 370 
Dicrotic pulse, 274 
Dietl's crises, 307 
Digestion, leukocytosis. 393 
Digestive disturbances cause of head- 
ache, 468 
of laryngeal spasm, 242 
Dilatation of heart, symptoms and 
physical signs of, 214, 259 
of pupil of eye, 412, 428 
of stomach, absence of hvdrochloric 
acid in, 299, 519 
atrophv of gastric tubules in, 

298 
constitution of vomitus in, 519 
examination in, 296, 298 
in pressure by growths of pan- 
creas. 519 
in tetany.: 4 * » 

^arcinae ventriculi in, 519 
Torula cerevisia-, 519 
vomiting in, 519 
x-rays in diagnosis of, 298 
Diphtheria, anesthesia in, 182 
breath in. 3 
casts of larynx and upper bronchial 

tubes at times coughed up in, 531 
diazo-reaction in, 370 
difficult swallowing due to paralysis 

from. 124 
double oculomotor paralysis in, 422 
glycosuria in convalescence from. 364 
involuntary passage of urine in, 332 
nasal. 127 

paralysis of tongue following. 122 
paraplegia a sequel to. 85 
roseola in. 148 

sickening sweet odor of breath in, 3 
symptoms of, 126. 127 
Diphtheritic dysentery, secondary. 320 

paralysis, dysphagia due to. 124 
Diplegia, spastic congenital, 70 
Diplopia, crossed. 415 
homonymous. 415. 418 
in meningitis. 413 
in poisoning. 413 

symptom of Friedreich's ataxia. 413 
of lesion at base of brain. 413 
of cerebral cortex. 413 
of cranial nerve nuclei. 413 
of nerve in its course. 413 
of locomotor ataxia. 413 
of paretic dementia. 413 
vertical. 418 
Dislocation, spontaneous, of the hip, 

following infectious diseases. 92 
Dissecting glossitis. 117 

-room diarrhea. 321 
Disseminated sclerosis, facial expres- 
sion in, 14 
Distoma hematobium in urine, 353 
hematuria due to, 338 



576 



INDEX 



Distoma pulmonum, 533 
Dittrich's plugs, 240 
Diverticulum of esophagus, 125 
Dropsy, 162. See Edema and general 
anasarca, 
general, in arsenic poisoning, 163 
in beriberi, 163 
in blood diseases, 162 
in cancerous cachexia, 163 
in disordered nervous control of 

vessels, 162 
in emboli, 162 
in heart disease, 163 
in multiple neuritis, 163 
in renal disease, 162 
in scurvy, 164 
in thrombi, 162 
in vascular disease, 162 
localized, in anemia, 163 
in aneurysm, 164 
in angioneurotic edema, 164 
in arsenic poisoning, 164 
in cardiac failure, 163 
in cerebral thrombosis, 164 
in hepatitis or cirrhosis, 163 
in mastoid abscess, 164 
in neuralgia, 164 

in occupations requiring a stand- 
ing position, 163 
in phlegmasia alba dolens, 164 
in pressure on great vein, 163 
in pyothorax, 164 
in relapsing fever, 164 
in renal disease, 163 
in thrombosis, 164 
in typhoid fever, 164 
of eyelids, 164 

of feet and legs in abdominal 
growths, 163 
in anemia, 163 
in cancer of pancreas, 163 
in renal disease, 163 
Dry rales, 222 
Dubini's chorea, 48, 506 
Dupuytren's contractions, 37 
Dynamometer, 58 

Dysentery, acute primary, of a diphthe- 
ritic character, 320 
amebic, Ameba coli cause of, 320 
liver abscess in, 320 
symptoms of, 320 
arthritis in, 91 

epidemic, due to Shiga's bacillus, 320 
fever in, 319 

secondary diphtheritic, in acute 
croupous pneumonia, 320 
in chronic heart disease, 320 
of Bright's disease, 320 
slight chill in, 319 
stools in, 319 
thirst in, 319 
tongue in, 116 



Dysentery, tropical, 319 

vomiting in, 517 
Dysmenorrhea, pain in, 550 
Dysphagia, causes of, 124 

due to stricture, 124 

in diphtheritic paralysis, 124 

in glossolabiopharyngeal paralysis, 
124 

in pharyngitis, 124 

in tonsillitis, 124 
Dyspnea from foreign body in air pas- 
sages, 242 

in anemia, 392 

in aortic insufficiency, 258 

in asthma, 242 

in chlorosis, 393 

in chronic interstitial nephritis, 373 

in heart disease, 12 

in laryngeal spasms, 242 

in leukemia, 395 

in miliary tuberculosis, 510 

in pneumothorax, 239 

inspection of chest in, 201 

position due to, 4 



Earache, character of crying in chil- 
dren with, 7 
rubbing of hand over affected side of 
head in, 7 
Echinococcus cysts of kidney, 307 

enlargement of gall-bladder due 
to, 292 
of liver, jaundice in, 133 
Echolalia, 27, 48 
Eclampsia, puerperal. See Puerperal 

eclampsia. 
Eczema, appearance of nails in, 35 
due to chloral, 155 
to mercury, 155 
to potassium iodide, 155 
to quinine, 155 
Edema. See also Dropsy and General 
anasarca, 
localized, 163 
neonatorum, 144 
of retina in general arterial disease, 

441 
of tongue, 120 

pulmonary, absence of fever in. 232 
crepitant and bubbling rales in, 

222 
due to disease of lungs, 232 

to injury of vagus, 232 
dulness on percussion in, 232 
feeble, hesitating speech in, 558 
in chronic interstitial nephritis, 

373 
position in, 5 
sputum in, 232 



INDEX 



577 



Edema, sputum in, liquid, watery, 530 
Effusion, pericardial, bulging of chest 
wall in, 196 
physical signs of, 215 
pleural, bronchial breathing in, 220, 
234 
accompanied by pneumothorax, 

physical signs of, 234 
bulging of chest-wall in, 195 
cryoscopy in, 238 
decreased vocal fremitus in, 205 

resonance in, 225 
displaced apex beat in, 205, 

206 
egophony in, 234 
flat percussior note over effusion, 

212, 233 
Grocco's sign in, 234 
hemorrhagic, 238 
physical signs of, 232, 233, 23 I 
seropurulent, absence of sugar in, 

285 
serous, Pohl and Rosenbach's test in, 
236 
sugar in, 285 

thrombosis of vena azygos cause 
of, 236 
skodaic resonance in, 212, 23 I 
tubercle bacilli in, determination of, 
238 
Egophony, 22(5 

in pleural effusion, 231 
Ehrlich, corpuscles of, 392 

diazo-reaction of, in urine, 370 
myelocyte of, 39 1 
triple blood stain of, 389 
Elbow-jerk, 58 
Electric chorea, 48, 506 

Bergeron's, 48 
Elephantiasis caused by Filaria san- 
guinis hominis, 405 
symptoms of, 143 
Embolism, cerebral, brachial monople- 
gia in, 52 
Cheyne-Stokes respiration in, 201 
gangrene in, 95 
hemiplegia in, 108, 109 
vomiting in, 509 
of coronary arteries, 264 
of kidnev, casts of, micrococci in, 
346 
edema in, 162 
hematuria in, 336 
of pons Varolii, 466 
Emphysema, barrel-shaped chest of, 
195, 240 
cardiac dulness in, 215, 240 
distended cervical vessels in, 202 
expiration prolonged in, 201, 240 
hands in, 34 

percussion resonance in, 240 
position in, 4 
37 



Emphysema, pulmonary and cardiac 
hypertrophy causing depression of 
apex beat in, 205 
rales in, 240 

spleen and liver displaced in, 240, 311 
systolic tricuspid murmur in, 240 
vocal fremitus in, 240 
resonance in, 225, 240 
Emprosthotonos in hysteria, 499 
Empyema communicating with bron- 
chus, loose morning cough in, 526 
in children, 238 
odor of breath in, 3 
organisms causing, 239 
peptonuria in, 360 
pulsation of chest wall in, 207 
purulent sputum in, 530 
symptoms of, 238 
Encephalomyelitis, 65 
Endarteritis, syphilitic, immobility of 

pupil in, 427 
Endocarditis, acute ulcerative, chill in, 
442 
diagnosis between typhoid fever 

and, 451 
duration of, 457 
fever in, 451, 457 
hematuria in, 335 
jaundice in, 135 
petechial rashes in, 142 
prognosis of, 457 
purpuric eruptions in, 141 
retinal hemorrhage in, 441 
sweating in, 161 
Enteric fever. See Typhoid fever. 
Enterocolitis, mild follicular, 319 
mucus in stools of, 318 
ribbon-shaped stools in, 318 
symptoms of, 318, 319 
ulcerative, 321 
Enteroliths, 324 
Eosinophilia, 396 
Eosinophil corpuscles, 383 

in trichinosis, 396 
Epidemic cerebrospinal meningitis, 
coma in, 490 
dvsenterv due to Shiga's bacillus, 
320 
Epigastrium, distention of, 285 

pulsation in region of, 204, 305 
Epilepsy, alcoholic, 495 
aura in, 491 

biting of tongue in, 119, 492 
caused bv drugs, 496 
by lead, 496 
by malaria, 497 
coma in, 490 
convulsions in, 491 
cutaneous hemorrhage in, 142 
diagnosis between attacks simulated 
b} r malingerers and, 502 
hysteria and, 498 



578 



INDEX 



Epilepsy, diagnosis between puerperal 
eclampsia and, 501 
syncope and, 502 
uremia and, 496, 500 
expression of face in, 491, 492 
facial spasm in, 27, 491 
fever after seizure of, 467, 500 
hippus in, 429 
idiopathic, 495 

Jacksonian convulsions in, 492, 493 
knee-jerk in, 553, 554 
lead, 496 
malarial, 497 

minor, diagnosis of, 501, 502 
unconsciousness in, 490 
vertigo in, 483 
muscse volitantes in, 436 
myosia at beginning of attack, 428 
nocturnal, headache due to, 482 
nystagmus a rare symptom of, 425 
posthemiplegic, 493 
scars on head in suspected traumatic, 

160 
syphilitic, 494 

diagnosis of, 494, 495 
symptoms of, 494 
tache cerebrale in, 144 
vertigo a premonitory symptom of, 
483 
Epileptiform convulsions from cerebral 
hemorrhage, 493 
from other causes, 493 
in cerebral palsy of children, 45 
Epiphysitis of infancy, 91 
Epithelial casts in urine, 345 
Epithelioma, ulcerati n of tongue in, 

118 
Equina. See Glanders. 
Erb's paralysis, 55 

symptom, 504 
Ergotism, gangrene in, 39, 157 

petechiae in, 142 
Eruption, date of, in various diseases, 
147 
from quinine, 155 
herpetic, in sciatic neuritis, 542 
in anthrax maligna, 156 

simplex, 156 
in chickenpox, 147, 154 
in erysipelas, 149, 156 
in glanders, 156 
in impetigo contagiosa, 155 
in measles, 146, 454 
in rheumatism, 140 
in rotheln, 145 
in smallpox, 146, 152, 454 
in syphilis, 159 
in typhus, 149, 452 
in vaccinia, 153 
of skin, 139 

pemphigus4ike, due to salicylic acid 
or copaiba, 157 



Eruption, pharyngeal and buccal, in 
measles, 146 

purpuric, from diseases, 140 
from drugs, 141 

vesicular, about mouth, in foot-and- 
mouth disease in man, 120 
Erysipelas, chill in, 442 

diazo-reaction in severe, 370 

edema of face in, 14 

eruption in, 149, 156 

fever in, 455 

inflammation of skin similar to, from 
arnica, 151 

peptonuria in, 360 

symptoms of, 149 

vomiting in, 523 
Erythema. See also Roseola. 

by drugs, 147, 150, 151 

exudativum multiforme, 142 

following operation, 149 
parturition, 149 
vaccination, 146 

in Bright's disease, 148 

in cholera, 148 

in dengue, 147 

in diabetes mellitus, 373 

in diphtheria, 148 

in German measles, 145 

in malaria, 148 

in measles, 146 

in rheumatism, 140 

in rotheln, 145 

in scarlet fever, 145 

in septicemia, 14 

in smallpox, 146 

in syphilis, 148 

in typhoid fever, 148 

roseola, symptoms of, 147 

scarlatiniform, symptoms of, 
148 
Erythrocytes, 374 
Esbach's test for albumin, 358 
Escherich's pseudotetanus, 504 
Esophagus, cancer of, 125 

diverticulum of, 125 

hysterical spasm of, 126 

spasmodic contraction of, 125 

stricture of, 124, 125 
diagnosis of, 125 
dysphagia due to, 124, 125 
Esophoria, 414 
Esthesiometer, 165 
Ewald's test breakfast, 299 
Exanthemata, date of eruption of 

various, 147 
Exhaustion from hiccough, 508 
Exophoria, 414 
Exophthalmic goitre. See Goitre, 

exophthalmic. 
Exophthalmos in thrombosis of caver- 
nous sinus, 480 
Expectoration. See Sputum. 



INDEX 



579 



Expression of face as an aid in diag- 
nosis, 3 
as an early symptom of facio- 
humeroscapular type of muscu- 
lar atrophy, 14 
elated, of paretic dementia, 14 
excited, of acute mania, 14 
fatuous, of hysteria, 14 
fixed, of catalepsy, 14 
how formed, 9 
how modified, 9 

in acute croupous pneumonia, 11 
fever, 12 
peritonitis, 13 
pulmonary phthisis, 12, 14 
in alcoholics, 10 
in cretinism, 15 
in croupous pneumonia, 11, 12 
in dyspnea of heart disease, 12 
iu epileptic seizures, 491, 492 
in Friedreich's ataxia, 15 
in healthy sleeping child, 1 1 
in hysteria, 14 
in malignant disease, 11 
iu melancholia, 14 
in moderate pain in children, 11 
in myxedema, L6, 17 
in nervous exhaustion, 14 
in paralysis agitans, 14 
in peritonitis, 1 1 
in renal disease, 14 
in typhoid fever, 13 
intellectual, 9 

of anxiety in grave disease, 11 
of "mouth breathers," 12 
variations in, 10 
External squint, causes of, 421 
Eye, alteration of color field of, 434 
amaurosis, 436 
annulus senilis, 412 
arcus senilis, 412 

conjunctival hemorrhage from 
coughing, 411 
from degenerative vascular 

changes, 411 
from injury, 411 
diagnosis between ocular symptoms 

of tabes and hysteria, 435 
diplopia, 412 
during menstruation, 10 
examination of, ophthalmoscopic, 

436 
exophthalmos in goitre, 411 

in lesion of oculomotor nerve, 22 
functional activity of muscles of, 414 
Graefe's symptom, 412 
hemianopsia, 431 
homonymous and crossed diplopia, 

415 " 
in cerebral facial paralysis, 19 
in locomotor ataxia, 440 
intra-ocular muscles of, 425 



Eye, iritis, 441 

musca; volitantes, 436 
orthophoria, 415 
papillitis, 439 
paralysis of, 416, 418 . 

muscles of, 41 3 
causes of, 419, 421 
puffiness about, from arsenic, 10, 411 

in acute diffuse nephritis, 372 
retinitis, 440 
retrobulbar neuritis, 440 
rod test of Maddox, 415 
squint, 413 

-strain, headache due to, 470 
Evelids, edematous, in angioneurotic 
edema, 143, 164 

from arsenic, 164 

in cerebral thrombosis, 164 

in neurotics, 164 
in health}' sleeping child, 11 
painful twitchings of, accompanying 

facial hemiatrophy, 16 
pallor of, in anemia, 411 
pigmentation of, in pregnancy, 10 
puffy, in cardiac disease, 1 1 1 

in overuse of arsenic, 411 

in renal disease, 10, 411 

in trichinosis, 14 
slightly parted in sleeping child, 

showing congestive or nervous 

pain, 11 
swollen, in cretinism, 15 

in trichiniasis, 14 
twitching. in nervous irritation, 11 



Face. See also Expression. 

and head, 9 

anesthesia of, diagnosis of, 185, 186 
due to involvement of the fifth 
nerve or its nucleus, 185 

asymmetry of, congenital, 16 

blurring of features of, in children 
with lesions of mitral valve, 13 

edema of, in dropsy, 14 
in erysipelas, 14 

expression of, 9 

an aid in diagnosis, 3 

faciohumeroscapular type of mus- 
cular atrophy, 14 

full-moon, of myxedema, 16, 17 

gray or bluish, from overdose of coal- 
tar products, 10 

heaw, cheesv-looking, in children, 
12 

hemiatrophy of, 16 

hemihypertrophy of, 17 

Hippocratic, of impending death, 14 

hysterical, 10, 14, 499 

in acute diffuse nephritis, 372 



580 



INDEX 



Face in angina pectoris, 540 
in leukemia, 395 
intellectual, 9 
leonine, of leprosy, 16 
massive, of acromegaly, 17 
of acute peritonitis, 13 
of carcinoma, 11 
of catalepsy, 14 
of cholera, 14 
of chorea in children, 14 
of chronic or subacute renal disease, 

14 
of congenital syphilis, 12 
of cretinism, 15 
of disseminated sclerosis, 14 
of exhausting disease, 14 
of Friedreich's ataxia, 15 
of leprosy, 16 
of paralysis agitans, 14 
of pneumonia, severe, 12 
of rickets, 12 

of those exposed to weather, 9 
living indoors, 10 
using alcohol in excess, 10 
of typhoid fever, 13 
pallor of, in chlorosis, 10 
in fright, 10 
in hemorrhage, 10 
paralysis of, bilateral, 25 

unilateral, 18 
parchment-like skin of, in syphilis 
and alcoholic hepatic cirrhosis, 10 
pellucid, in renal disease in children, 

14 
spasm of, 26 

triangular, in osteitis deformans, 17 
Facial deformity, 16 

expression from nasal obstruction, 12 
paralysis, bilateral, 25 

unilateral, 18 
spasm, 26 
Family idiocy, amaurotic, 70 

periodic paralysis, 85 
Farrant's solution, 350 
Fat, masses of. See Adiposis dolorosa, 
necrosis from impacted gallstone, 304 
Fatty casts in urine, 347 

degeneration in phosphorus poison- 
ing, 521 
diarrhea, 321 
heart, 264 
Fecal calculi, 324 
Feces. See also Stools, 
color of, 322 
consistency of, 321 
impaction of, 306 

pain in, 547 
odor of, 322 

variation in quantity of, 321 
Feet and legs, deformities of, 88 

physical methods in examining, 97 
claw-, 74 



Feet, contractures of, in hysteria, 45 
deformity of, due to acute cerebral 
paralysis of infancy, 75 
to poliomyelitis, 87 
to progressive muscular atrophy, 
89 
distribution of anesthesia of, in neu- 
ritis, 185 
enlarged, due to deformity, 88 
in acromegaly, 88 
in myxedema, 88 
in pulmonary osteo-arthropathy, 
88 
flat-, in locomotor ataxia, 89 
numbness of, in locomotor ataxia, 60 
perforating ulcer of, in diabetes, 95 
in senile gangrene, 95 
in tabes dorsalis, 95 
sciopedy, 88 
tabetic, 88 
Fehling's test for sugar in the urine, 361 
Femur, malignant growth of, diagnosis 

of, from sciatica, 541, 542 
Festination, 67, 505 
Fever, 442 

absence of, in pulmonary edema, 232 
cold, wet skin of evil import in, 445 
Charcot's, 132, 457 
chlorides decreased in some, 370 
increased during convalescence 
from, 370 
drv, hot skin in, 445 
flushed face in, 12, 445 
high specific gravity of urine in, 343 
in acute appendicitis, 289 
in anthrax, 156 
in articular rheumatism, 465 
in bronchitis, 465 
in catarrhal pneumonia, 465 
in cerebral abscess, 510 
in cerebrospinal meningitis, 461 
in chickenpox, 455 
in chlorosis, 393 

in cholangitis, catarrhal or sup- 
purative, 457 
in cholera Asiatica, 316 

infantum, 316 
in croupous pneumonia, 464 
in dengue, 460 
in difficult dentition, 446 
in dysentery, 319 
in epilepsy, 467, 500 
in erysipelas, 455 
in foot-and-mouth disease, 120 
in hemoglobinuria, 522 
in hay fever, 464 
in hepatic abscess, 457 
in Hodgkin's disease, 459 
in hysteria, 467 

in infantile spinal paralysis, 84, 87 
in infectious diseases, 446 
in influenza, 467 



INDEX 



581 



Fever in injuries to spinal cord, 467 

in intermittent malarial fever, 456 

in leukemia, 395 

in Malta fever, 452 

in measles, 454 

in mild gastro-intestinal catarrh in 
children, 446 

in miliary tuberculosis, 404 

in multiple neuritis, 466 

in pemphigus, 157 

in pernicious anemia, 459 

in pulmonary tuberculosis, 403 

in pyelitis. 342, 159 
suppurative, 459 

in relapsing fever, 452 

in remittent malarial fever, 459 

in rotheln, 454 

in scarlet fever, 453 

in septic poisoning, 459 

in septicemia, 463 

in smallpox, 454 
secondary, 152 

in syphilis, 465 

in teething, I Hi 

in thermic fever, 466 • 

in tonsillitis, 126 

in trichinosis, 452 

in typhoid fever, 446 

in typhus fever, 452 

in ulcerative endocarditis, 451 . 457 

in Weil's disease, 459 

in yellow fever, 460 

infantile remittent, 459 

nails in, 35 

rapid pulse in, 277 
respiration in, 200 

septic, in purulent cystitis, 329 

sighing or arhythmic respiration in, 
in children. 8 

tertian, quartan, and estivo-autum- 
nal, 396, 39!) 

thermic, 466 

urates in excess in urine of, 350 

urea increased in urine of, 309 

urethral, from passing sounds, 446 

uric acid increased in urine of, 351 

urine decreased in, 334 
Fibrinous bronchitis, small casts of 

bronchial tubes in sputum in, 531 
Fibroid phthisis, inspection of chest in, 

230 
Filaria demarquayi, 404 

diurna, 403 

embryos of, in urine, 338, 353 

hematuria in, 338 

loa, 404 

nocturna, 403 

ozzendi, 404 

perstans, 403 

sanguinis hominis in blood, 403 
chyluria and elephantiasis 
caused by, 405 



Filaria sanguinis hominis, hematuria 

due to, 338 
Fingers, appearance of, diagnostic of 
chloral habit, 35 
clubbed, in heart disease, 34, 258 
fixation of joints of, 30 
in gout and arthritis deformans, 3G 
in syphilitic dactylitis, 35 
spasm of, due to occupation, 40 
"Fish-mouth" of nasal obstruction, 12 
Fissure of the anus, diarrhea in, 318 

pain in, 550 
Flatfoot in locomotor ataxia. 89 
Flint's murmur, 250 
Floating kidney, 306 
pain in, 547 
liver, 303 
spleen, 312 
Fluoroscope in diagnosis of aortic aneu- 
rysm, 255 
of tuberculosis, 231 
Follicular enterocolitis, mild, 319 

tonsillitis, symptoms of, 126 
Fontanelle, condition of, diagnostic, 

31, 32 
Foot-and-mouth disease in man, erup- 
tion in, 120 
Foot-drop, 87 

Forehead, immense and bulging, with a 
wizened, puny face beneath, indi- 
cating hydrocephalic tendencies, 
12 
square and projecting, in rickets, 12 
wrinkled, indicating pain in head, 
12 
Foreign bodv in air passages, 242 

in bowel, 306 
Formication, 62, 168 
Fovea centralis, 438 
Fremitus, vocal, decrease of, 205 
increase of, 205 
mode of production of, 204 
Friction sounds, 223 

at apex of chest, due to tubercu- 
losis, 224 
due to pleuritis, 223 
heard in axilla, 224 
pericardial, 223, 257 
, Friedreich's ataxia, clawfoot in, 75 
diagnosis of, 554 

differential, between locomotor 
ataxia and, 63, 64 
diplopia a symptom of, 413 
face of, 15 
gait of, 59, 63 
knee-jerk in, 553 
movement of hands in, 51 
nystagmus in, 425 
sensory disturbance of skin in, 174 
slow, scanning speech in, 559 
Frog-belly, 280 
Frostbite, gangrene in, 39 



582 



INDEX 



Fungus foot disease, 95. See Myce- 
toma. 

Furunculosis, 156 

in diabetes mellitus, 373 



Gabbett's method of staining for tu- 
bercle bacilli, 535 
Gait, 59 

"astasia abasia," 68 

in acute poliomyelitis, 66 

in cerebellar disease, 67 
tumor, 68, 474 

in chronic myelitis, 65 

in disseminated sclerosis, 64 

in Friedreich's ataxia, 63 

in general paresis, 63 

in gout, 59 

in health, 2 

in hemiplegia, 68 

in hereditary cerebellar ataxia, 64 

in Huntingdon's chorea, 506 

in hysteria, 68 

in infantile cerebral paralysis, 66 

in lateral sclerosis, 66 

in locomotor ataxia, 59, 64 

in multiple sclerosis, 65 

in neurasthenia, 2 

in osteomalacia, 68 

in paralysis agitans, 67 

in pseudomuscular hypertrophy, 66 
-tabes, 60 

in rheumatism, 59 

in rickets, 66, 69 

in sciatica, 59 
Gall-bladder, cancer of, 292 

diagnosis of obstruction of, 292 

hydrops of, 292 
Gallop rhythm in mitral stenosis, 249 
Gallstone colic, 293, 304, 543 

in catarrhal or suppurative cho- 
langitis, 457 
in stools, 324 
jaundice in cases of, 131 
Gallstones, enlargement of gall-bladder 

due to, 293 
Gametocytes, 401 
Gangrene in central nervous lesion, 157 

diabetic, of toes, 95 

in diabetes, 158 

in embolism, 95 

in ergotism, 39, 157 

in exophthalmic goitre, 95 

in frostbite, 39 

in leprosy, 39 

in nerve injury, 157 

in Raynaud's disease, 39, 158 

of extremities, following infectious 
fevers, 95 
in diabetes mellitus, 373 



Gangrene of intestines, odor of stools 
in, 322 
pulmonary, due to putrid bronchitis, 
240 
fetid breath in, 3, 232 
mucopurulent stools in, 321 
sputum in, 232, 529, 530 

crystals of margaric acid in, 532, 

533 
elastic fibers in, 532 
vomiting in, 523 
senile, perforating ulcer of foot in, 95 
spontaneous, in hysteria, 157 
Gastralgia, diagnosis of, 550 
neuralgic spots in, 550 
pain in, 549 
position in, 4 
Gastric cancer, anemia in, 391 
fever in, 459 
indicanuria in, 341 
most frequent at pylorus, 290 
vomiting in, 290, 517 
catarrh, acute, tongue in, 115 
vomiting in, 518 
chronic, vomiting in, 519 
crisis in locomotor ataxia, 60 
dilatation, 295. See Dilatation of 

stomach, 
disorders, odor of breath in, 3 
ulcer, anemia in, 291, 391 
pain in, 291, 541, 551 
vomiting of blood in, 517 
Gastritis, vomiting in, 519 
Gastrodiaphane of Einhorn, 296 
Gastroduodenal catarrh, jaundice in, 

131 
Gastroptosis, Glenard's belt sign of, 298 

jaundice as result of, 133 
General anasarca in acute diffuse ne- 
phritis, 372 
in advanced cancerous cachexia, 

163 
in arsenic poisoning, 163 
in beriberi, 163 

in children with acute diffuse ne- 
phritis, 372 
in chronic parenchymatous ne- 
phritis, 372 
in heart disease, 163 
in multiple peripheral neuritis, 163 
in renal disease, 162 
Geographical tongue, 120 
Gerhardt's symptom, 480 
German measles. See Rotheln. 
Girdle sensation, 188 

in locomotor ataxia, 188 
in transverse myelitis, 74, 77, 188 
in tumors of cord and meninges, 
188 
Glanders, eruption of, 156 
Glaucoma, dilated pupil in, 412 
headache in, 471 



INDEX 



583 



Glenard's belt sign of gastroptosis, 298 
Globus hystericus in hysteria, 499 
Glossitis, acute, 120 
chronic superficial, 119 
dissecting, 117 
Glossodynia, exfoliativa, 119 
Glossolabiopharyngeal paralysis, 25 
cardiac feebleness in, 264 
cough in, 527 
dysphagia in, 124 
tongue in, 121, 123 

bilateral atrophy of, 120 
Glycosuria, Fehling's test for, 361 
Haines' test for, 361 
phenylhydrazin test for, 363 
Roberts' yeast test for, 363 
Trommer's test for, 363 
Whitney's test for, 361 
Gmelin's test for bile in urine, 341, 365 
Goitre, exophthalmic, Abadie's sign in, 
27, 33 
brown pigmentation in, 137 
electrical resistance in, 263 
exophthalmos in, 33, 411 
gangrene in, 95 
Graefe's symptom of, 412 
leucoderma in, 138 
localized sweating in, 161 
Moebius' sign of, 412 
paroxysmal bloody, mucous diar- 
rhea in, 321 
Stell wag's symptom in, 412 
symptoms of, 411 
tache cerebrale in, 144 
tachycardia in, 33, 263 
thrill over carotid arteries in, 263 
tremor of hand in, 50 
vomiting in, 522 
Gonococci a cause of empyema, 239 
indicative of specific urethritis or 

vaginitis, 354 
method of staining, 354 
Gonorrheal arthritis, acute, 89 
Gout, aortitis in, 540 
fingers in, 36 

hyperesthesia of scalp in, 189 
joint affections in, 92 
limping gait of, 59 
nails in, 36 

pain in great toe in, 550 
plumbic, 92 
pruritus in, 190 
retinal hemorrhages in, 441 
urine of, 350 
Gouty diathesis, nails in, 35 
Graefe's spots, 27 
symptom, 412 
Granular casts in urine, 346 
Graves' disease, tremor of hand in, 50 
Gravid leukocytosis, 393 
"Grisolle" sign of smallpox, 147 
Grocco's sign in pleural effusion, 234 



Groins, 313 

Guaiacum test for hemoglobin, 360 
Gumma, syphilitic, 474 
Gums, blue line on, in lead poisoning, 
124 
spongy, in salivation, 124 
in scurvy, 124 



Habit chorea, 47 

spasm, 26, 47 
Hands, "accoucheur's," in tetany, 45 

and arms, 34 

general movements of, 51 
physical examination of, 58 
tremors of, 49 

changes in shape of, in amyotrophic 
lateral sclerosis, 44 
in chronic rheumatism, 38 

choreic movements of, in children 
with chorea minor, 47 

claw-, 40 

in Morvan's disease, 43 

cold and clammv, due to bromidro- 
sis, 36 ' 
to local innervation of sweat 
glands, 36 

contractions of, following apoplexv, 
45 
from hysteria, 45 

distribution of anesthesia of, in neu- 
ritis, 184 

Dupuytren's contraction of, 37 

flexion of, in cerebral palsy of chil- 
dren, 44 

gangrene of, 39 

in acute articular rheumatism, 38 

in angioneurotic edema, 39 

in child with cerebral trouble, 8 
with heart disease, 34 

in emphvsema and chronic phthisis, 
34 

in heart disease, 4 

in meningeal congestion or hydro- 
cephalus in children, 45 

in thoracic aneurysm, 34 

inspection of, 34 

lateral drop of, in neuritis or acute 
infantile poliomyelitis, 46 

seal-fin, in arthritis deformans and 
gout, 37 

spade-like, 40 

spasm of, 48 

sweating of, in progressive muscular 
atrophy, 36 

swelling and rupture of, 40 

tremors of, 49 

wasting of, 40 

with flexion and rigidity rarely 
seen in paralysis agitans, 44 



584 



INDEX 



Harrison's grooves in rickets, 198 
Haut mal, 501 
Hay fever, 464 
Haygarth's nodosities, 37 
Head, examination of, 28 

excessive sweating of, 33 

in acromegaly, 30 

in advanced strabismus, 30, 416 

in cholera infantum, 316 

in chorea minor, 29 

in chronic deafness, 30 

in cretinism, 30 

in hydrocephalus, 30 

in idiocy, 30 

in mental depression, 30 

in microcephalus, 30 

in myxedema, 30 

in osteitis deformans, 30 

in peritonitis, 4 

in rickets, 30, 33 

neuralgia of, 537 

retraction of, 30 

tremor in disseminated sclerosis, 50 
Headache, causes of, 468 

due to chloral habit, 471 
to hemorrhage, 482 

from use of drugs, 471 

in anemia, 482 

in anterior poliomyelitis, 83 

in auto-intoxication, 470 

in brain abscess, 476 
tumor, 472, 509 

in cerebral tumors, 509 

in cerebrospinal meningitis, 461 

in croupous pneumonia, 481 

in dental caries, 483 

in diabetes, 472 

in digestive disturbances, 468 

in disease of cranial bones, 482 

in ear disease, 483 

in exposure to cold, 483 

in eye-strain, 470 

in glaucoma, 471 

in hematoma of the dura, 480 

in hemoglobinuria, 469, 470 

in intermittent fever, 482 

in intracranial aneurysm, 482 

in iritis, 471 

in jaundice, 469 

in malaria, 482 

in Malta fever, 452 

in measles, 482 

in meningeal hemorrhage, 480 
tumors, 472 

in meningitis, 476, 510 

in migraine, 469 

in nasal catarrh, 482 

in neurasthenia, 471 

in nocturnal epilepsy, 482 

in paroxysmal hemoglobinuria, 469 

in phosphaturia, 471 

in phosphorus poisoning, 521 



Headache in renal disease, 471 
in rheumatism, 471 
in smallpox, early stages, 481 
in sunstroke, 481 
in syphilitic arteritis, 474, 475 

epilepsy, 494 

gumma, 474, 475 

meningitis, 474, 475 
in tuberculous meningitis, 476 
in typhoid fever, 482 
in typhus fever, 452 
in uremia, 471, 472 
in valvular heart disease, 482 
vomiting in, 522 
Heart, alterations in area of dulness of, 

214 
apex beat of, 205, 206 

displacement of, to left, 206 
to right, 206 

raised, 206 

strength of, 206 
asthma due to lesions of, 241 
blood-streaked sputum in valvular 

lesions of, 529 
causes of pain in neighborhood of, 

539 
congenital malformations of, 255 
cough in valvular disease of, 526 
dilatation of, 207, 214, 259 

in acute diffuse nephritis, 372 
disease of, appearance of hands in 
children in, 34 

cyanosis in, 139 

edema in, 163 

hematemesis in, 518 

jaundice in chronic valvular, 133 

patient's position in, 4, 5 

retinitis in, 440 
failure, in influenza, 262, 464 

unconsciousness in, 490 
fatty degeneration of, 264 

deposition on, 264 
general malformation of, 255 
headache in valvular disease of, 482 
hypertrophy of, 262 

in chronic parenchymatous ne- 
phritis, 372 
in chronic interstitial nephritis, 372 
location of murmurs of, 246 
murmurs, significance of, 246 
neuroses of, 263 
percussion of, 213 
secondary diphtheritic dysentery in 

chronic disease of, 320 
sounds, 244 

accentuation of, 245 

normal, 244 

reduplication of, 246 

where best heard, 245 
symptoms associated with murmurs 

of, 255 
thrills of, 207 



INDEX 



585 



Heart, tobacco, 203 

valvular lesions of, 255, 257 
Heat exhaustion, subnormal tempera- 
ture in, 407 

stroke. See Sunstroke. 

prostration, diarrhea due to, 317 
Heherden's nodes, 37 
Heel and toe, tender, in sciatica, 542 
Heller's test for albumin in urine, 350 

for blood in urine, 300 
Hematemesis, as vicarious menstrua- 
tion, 518 

diagnosis between hemoptysis and, 
518 

due to swallowed blood, 518 

in acute yellow atrophy of liver, 518 

in cirrhosis of liver, 518 

in dengue, 518 

in gastric cancer, 517 
ulcer, 517 

in heart disease, 518 

in hemophilia, 518 

in influenza, 5 1 8 

in injury of stomach, 518 

in locomotor ataxia, 517 

in malaria , 5 1 8 

in melena neonatorum, 518 

in purpura hemorrhagica, 518 

in relapsing fever, 518 

in scurvy, 518 

in typhus fever, 518 

in yellow lexer, 518 
Hematocrit, 380 

Hematooytometer of Thoma-Zeiss, 370 
Hematogenous jaundice, 134 
Hematoma auris, 142 

of dura, headache in, 480 
mater, convulsions due to, 504 

subperiosteal, in children, 91 
Hemoglobin, 385 

diagnosis of syphilis by, 393 

estimation of, 385 

in chlorosis, 392 

in leukemia, 39 1 

specific gravity of, 388 
Hemoglobinometer, Dare's, 385 

von Fleischl's, 385 
Hematozoa malaria 1 , 390 
Hematuria, acute, 330 

blood casts in, 340 
from bladder in, 335 
from kidney in, 335 
from urethra in, 335 

chronic, 337 
Hemiachromatopsia, 435 
Hemianesthesia due to lesion of optic 
thalamus, 170 

in apoplexy, 170 

in capsular disease, 109, 170 

in chorea, 170 

in cortical lesions, 170 

in disseminated sclerosis, 170 



j Hemianesthesia in hysteria, 169 
in softening of brain, 170 
in tumor of brain, 170 
partial, with partial hemiplegia on 
opposite side, due to lesions of one 
side of cord, 172 
Hemianopsia, 428, 431 
binasal, 432 
bitemporal, 432, 434 
homonymous, 432, 433 
in brain tumor, 473 
in hysteria, rarely, 109, 434 
in migraine, 538 
location of lesion in, 432 
method of determining, 432 
use of perimeter in determining, 432 
Hemiatrophy, facial, 10 

of tongue, 121 
Hemicrania. See Migraine. 
Hemidyschromatopsia. 135 
homonymous, 435 
in hysteria, 435 
llemihypertrophy, facial, 17 
Hemilateral myelitis, symptoms of, 80 
Hemin, test for, 524 
Hemiopic pupillary inaction. 128, 173 
Hemiplegia, bed-sores in, 158 
brain areas involved in. 99 
crossed, due to bulbar lesions, 110 
diagnosis of, 105 

from acute infantile paralysis, 109 
from cerebellar hemorrhage, 108 
from cerebral hemorrhage, 104 
in crus cerebri, 111 
in frontal lobe, 106 
in internal capsule, 105 
in island of Reil, 108 
in occipital lobe, 106 
in parietal lobe, 105 
in pons Varolii, 110 
location of lesion in, 105 
syphilis, 109 
from diffuse cerebral sclerosis of one 

hemisphere, 109 
from disseminated sclerosis, 109 
from hematoma of dura mater, 109 
gait in, 08 

hyperesthesia in, 189 
in cerebral embolism, 108, 109 

thrombosis, 108 
in ingravescent apoplexy, 100 
in locomotor ataxia, 109 
in paretic dementia, 110 
in purulent meningitis, 110 
in renal disease with uremia, 110 
irregular forms of, 108 
nails in, 35 

pupillary immobility in, 427 
spastic, 109 

infantile, 44 
symptoms associated with, 104, 105, 
100 



586 



INDEX 



Hemiplegia, tongue in, 116 
Hemoglobin decreased in chlorosis, 392 

in leukemia, 394 
Hemoglobinometer, Dare's, 387 

von FleischFs, 385 
Hemoglobinuria, paroxysmal, 340 

signs of, 340 

symptoms associated with, 469 

urine in, 522 

vomiting in, 522 
Hemometer. See Hemoglobinometer. 
Hemophilia, 338 

hematemesis in, 518 

hematuria in, 338 

hemoptysis in, 529 

hemorrhage into retina in, 441 

joint involvements in, 92 
Hemoptysis, currant-jelly clots in, 529 

diagnosis of, 518, 529 
Hemorrhage, anemia in, 391 

cerebellar, 108 

cerebral, causing hemiplegia, 104 
ocular paralysis, 419 
glycosuria after, 364 
hiccough in, 508 
diplopia a symptom of, 413 
vomiting in, 509 

facies in, 14 

from mucous membrane in yellow 
fever, 460 

from nose in leukemia, 395 

from stomach, 518 

in Banti's disease, 311 

in typhoid fever, 447 

indicated by anxious restlessness, 4 

into lesser peritoneum, 304 

into membranes of cord, 76, 174 

into retina, 440 

into skin, 142 

into spinal cord, 75 
paraplegia in, 75 

jaundice after severe prolonged, 134 

meningeal, symptoms of, 107, 480 

pallor of face in, 10 

pulmonary diseases in which it oc- 
curs, 529 

pulse of "empty arteries" in severe, 
275 

subdural, cause of, 489 

ventricular, differential diagnosis be- 
tween meningeal hemorrhage, 107 
Hemorrhagic infarction of intestine, 
304, 515 

pleural effusion, 238 

pleurisy, 238 

smallpox, hemoptysis in, 529 

retinitis, 440 
Hemorrhoids, anemia in bleeding, 391 

blood in stools caused by, 322, 323 

pruritus due to, 190 
Henoch's disease, 141 
Hepatic abscess, fever in, 457 



Hepatic abscess, tongue in, 116 

cirrhosis, enlargement of spleen in, 
310 
hematemesis in, 518 
jaundice in, 132 
with pigmentation, 134 
colic, 131, 543 

retraction of abdominal wall in, 
281 
disease, constipation in, 314 
Hepatitis. See Abscess, hepatic. 
Hepatogenous jaundice, 170 
Hernia, umbilical, 287, 309 
Herpes labialis after salicylic acid, 155 
in croupous pneumonia, 12, 155 
in epidemic spinal meningitis, 155 
zoster, 156 
Hiccough, 508 
Hip disease, pain in, 6, 541 

spontaneous dislocation of, following 
infectious disease, 92 
Hippocratic face, 14, 316 

succussion, 226 
Hippus, 429 

Hodgkin's disease, differential diagnosis 
of, from true leukemia, 395 
enlargement of cervical lymphatic 

glands in, 33, 459 
temperature in, 459 
Holland's test for indican, 365 
Hollow chest an indication of tubercu- 
losis, 2 
Hour-glass stomach, 299 
"Humming-top" murmur in chlorosis, 

393 
Huntingdon's chorea, 48, 506 
Hutchinson pupil in cerebral hemor- 
rhage, 107 
teeth, 124 
Hyaline casts in urine, 347 
Hydatid cyst of liver, 304 

disease of spleen, 312 
Hydrarthrosis, chronic, 89 
Hydrocephaloid disease, 503 

state, 32 
Hydrocephalus, contraction of hands 
and arms in, 45 
face in, 12 
head in, 30 
nystagmus in, 425 
open fontanelle in, 30, 31 
spastic rigidity of arms in, 46 
Hydrochloric acid, test for, in stomach 

contents, 299 
Hydronephrosis, 308 
Hydropneumothorax, coin percussion 
in, 235 
Hippocratic succussion in, 226 
metallic tinkling in, 222 
physical signs of, 234, 235 
Hydrops of gall-bladder, 292 
Hyperesthesia, 188 



IXDEX 



587 



Hyperesthesia following the use of 
drugs, 189 
in anemia, 189 
in brain t umor, 1 89 
in cerebrospinal meningitis, 188 
in chronic alcoholism, 189 

leptomeningitis, 189 
in gout. 189 
in hemiplegia, 189 
in hysteria, 169, 188 
in influenza, 189 
in leprosy, 189 
in locomotor ataxia, 188 
in menopause, 189 
in myelitis, 188 
in neuralgia, 189 
in neurasthenia, 188 
in peripheral neuritis, 188 
in poisoning by lead and arsenic, 189 
in relapsing fever, 189 
in rickets, 189 
in scurvy, 189 
in transverse myelitis, 188 
in typhoid fever at convalescence, 

189 
Hyperpyrexia, 442 

Bypertrophy, cardiac, apex beat in. 
205 

associated with chronic contracted 
kidney, increase of urine in. 334 

diagnosis of, 262 

in chronic interstitial nephritis, 
372 

limited bulging of chest in. 1'.).") 
of nails in. 35 

pulse in, 276 

pseudomuscular gait in. 66 

symptoms and signs of. 262 
Hypotonus in locomotor ataxia, (51 
Hysteria, allochiria in. 187 

alterations of color fields in. 434 

anesthesia in, 168 

aphonia in. 557 

bilateral anesthesia in. 172 

brachial monoplegia in, 53 

bromidrosis in, 101 

contractions of hands, feet, and legs 

in, 45 
convulsions in, 498 
diagnoses of, 49S, 503 
diarrhea in. 321 
dilated pupil in. 412 
emprosthotonos in, 499 
facial paralysis in, 20 

spasm in, 28. 499 
false clonus in. 555 
fatuous expression in. 14 
fever in, 467 
gait in paralysis of, 68 
gauntlet or stocking form of anes- 
thesia in, 171 
globus hystericus in, 499 



Hysteria, hemianesthesia in, 169. 134 
hemianopsia rare in. 169, 434 
hemidyschromatopsia in. 435 

hemorrhages into skin in, 142 

hiccough in. 508 

hippus rare in, 429 

hysterogenous zones of hyperesthe- 
sia in, 188 

localized sweating in. lid 

mirror writing rare in, 52 

nodding spasm in, 28 

ocular symptoms of, 435 

opisthotonos in. 499 

pain, cutaneous, in, 190 

painful joints in. 542 

paraplegia in, 69, 84 

phantom tumor in. 3D!) 

ptosis in, 24 

respirations in. 200 

spasm of esophagus in. 125 
of tongue in. 123 

spontaneous gangrene of skin in, 157 

squint in. 425 

status epilepticus in. 498 

subnormal temperature in. 407 

tremor of hands in. 50 

urine increased in. 334 

visual changes in. 169 

vomiting in. 520 

wryneck in, 29 
Hysterical chorea, 1^ 

mutism. 557 

paralysis, 68 
Hystero-epilepsy, diagnosis of. olio 
Hysterogenous zones, 188 



"Iced" liver. 303 
Ichthyosis of tongue. 119 
Icterus. See Jaundice, 
neonatorum. 135 
urobilin. 134 ' 
Idiocy. 30 

amaurotic family. 70 
Idiopathic epilepsy, 495 
Idiosyncrasy to drugs, 2. 141 

hemoglobinuria of. 338 
Impaction of feces. 306 
Impetigo contagiosa, eruption in. 155 
Incontinence of urine, 2 

due to concentrated urine. 332 
to excessive reflex irritation of 

bladder walls. 332 
to insensitive urethra. 332 
to loss of power of sphincter, 332 
erythema of thighs in, 150 . 
nocturnal, in children, 332 
trousers stained in. 2 
Incubation period of eruptive diseases. 
147 



588 



INDEX 



Indicanuria, 3G5 

diseases in which it occurs, 341 
test for, 341, 365 
Indigestion, acute, roseola of, 147 
anemia in chronic, 390 
headache associated with, 468 
hiccough in, 508 
intestinal pain in, 544 

muscse volitantes in, 436 
respiration of child with, 8 
retraction of head in neurotic chil- 
dren with, 30 
vertigo in, 483 
Infantile cerebral paralysis, gait in, 
66 
movements of hand in, 51 
hemiplegia, spastic, 44, 109 
remittent fever, 459 
spinal paralysis. See Anterior polio- 
myelitis. 
Infarction, hemorrhagic, of intestine, 
304, 515 
pulmonary, hemoptysis in, 529 
renal, blood casts in, 346 
hematuria in, 336 
Influenza, epidemic, cardiac failure in, 
464 
catarrhal symptoms of, 464 
complications of, 464 
diarrhea, 464 
differential diagnosis from dengue, 

460 
fever in, 464 
glycosuria in convalescence from, 

364 
hematemesis in, 518 
hyperesthesia in, 189 
microorganism of, as cause of em- 
pyema, 239 
ocular palsy in, 421 
pain in back in, 551 
sputum in, 530 
vomiting in, 464 
Ingravescent apoplexy, 106 
Inoscopy, 238 

Insomnia in Malta fever, 452 
Inspection of chest, 191 

of abdomen, 280 
Interlobular pleurisy, physical signs of, 

238 
Intestinal crises in locomotor ataxia, 
318 
hemorrhage in typhoid fever, 447 
indigestion, pain in, 544 
obstruction, 306 

albumin in urine, 514 
constipation in, 315 
due to cancer or stricture, 515 
to impaction of foreign body, 

515 
to intussusception, 512 
to strangulation by bands, 513 



Intestinal obstruction due to strangu- 
lation by Meckel's diverticu- 
lum, 514 
to volvulus, 515 
hiccough in, 508 
indicanuria in, 341 
leukocytosis in, 396 
parasites, 324 
perforation, pain in, 546 
rigidity, 309 

vomit in, 523 
sand, 324 
Intestine, hemorrhagic infarction of, 

515 
Intra-ocular muscles, paralysis of, 425 
Intussusception, sloughing of bowel in, 

324 
Iodophilia, 396 

vomiting in, 511 
Iritis due to injury, 441 
to rheumatism, 441 
to syphilis, 441 
headache due to, 471 
immobile pupil in, 412 
Irregular breathing, 220 
Irritative mydriasis, 428 

myosis, 428 
Itching of jaundice, 134, 190 



Jacksonian epilepsy, 492 
Jacquet's sphygmocardiograph, 276 
Jaundice, 130 

as result of gastroptosis, 133 

bradycardia in, 263 

catarrhal, 131 

Charcot's fever in, 132 

diabete bronze in, 133 

fatty diarrhea in, 321 

from cerebral concussion, 136 

from fright or extreme anger, 136 

hematogenous, 134 

headache in, 469 

hepatogenous, 130 

in acute phosphorus poisoning, 133 
ulcerative endocarditis, 135 
yellow atrophy, 134 

in amyloid liver, 133 

in cholangitis, 457 

in chronic valvular heart disease, 133 

in cirrhosis of liver, 132 

in croupous pneumonia, 135 

in diabetes, 133 

in disease of pancreas, 133 

in echinococcus of liver, 133 

in malignant disease, 132 

in newborn, 135 

in pressure from aneurysm, 131 

in remittent malarial fever, 459 

in Weil's disease, 133, 460 



INDEX 



589 



Jaundice in yellow lexer, 133, 460 

itching of, 134 

obstructive, 131 

peptonuria in, 360 

persistent and progressive in carci- 
noma of pancreas, 294 

pruritus in, 134, 190 

purpuric eruption in severe, 141 

pyemic, 135, 136 

stools in, 134, 322 

sweating in, 161 

tongue in, 114 

urine in, 134, 339, 340 

vomiting in, 522 
Joints, 89 

alterations of, 90 

hypertrophic osteoarthritis following 
typhoid fever, 91 

in acute epiphysitis of infancy, 91 
synovitis, 90 

in central myelitis, 89 

in cerebrospinal meningitis, 89, 91 

in chronic lead poisoning, 92 

in dengue, 92 

in gonorrheal arthritis, 89 

in gout, 92 

in hemophilia, 92 

in milk leg, 93 

in osteomyelitis, 91 

in rheumatoid arthritis, 90 

in scarlet fever, 93 

in Schonlein's disease, 92 

involvement of, with fever, 466 

pain on motion of, in Malta fever, 452 

small, in Morvan's disease, 89 
in syringomyelia, 89 
Jumpers, the, 48, 507. See Saltatoric 

spasm. 



Kernig's sign in meningitis, 479 
Kidney, blood casts in acute inflam- 
mation of, 346 

blood in urine from, 335, 337 

cancer of, hematuria due to, 337 

chronic contracted, accentuation of 
heart sounds in, 245 

cystic degeneration of, 307 

fatty casts in fattv degeneration of, 
347 

floating, 306 

hematuria due to stone in, 337 

hydronephrosis, 308 

irritation of, cvlindroids found in, 
348 

methylene-blue test to determine 
activity of, 344 

multiple abscess of, pus casts in 
urine in, 346 

pain in, 547 ' 



Kidney, septic infection of, casts of 
micrococci in, 346 
hematuria due to, 336 
slow degeneration of parenchyma of, 

granular casts in, 347 
tuberculosis of, 337, 548 
Klumpke's paralysis, 55 
Knee-jerk, diseases in which it is de- 
creased, 553 
in which it is increased, 554 
how best elicited, 552 
in locomotor ataxia, 60 
reinforced, 552 
testing of, 97 
Kyphosis, 17 



La grippe. See Influenza. 
Lactic acid, test for, in stomach con- 
tents, 299 
Landouzy-Dejerine type of muscular 

atrophy, 14 
Landry's paralysis, diagnosis of, 7(i, 160 
from acute central myelitis, 7(1 
loss of knee-jerk in, 553 

of reflexes, predominant symp- 
tom of, 466 
non-spastic paraplegia in, 76 
Laryngeal crises in locomotor ataxia, 
60 
obstruction, cyanosis due to, 139 
paralysis, 558 
phthisis, cough in, 527 
spasm, 242 
Laryngismus stridulus in tetany, 504 
Laryngitis, night cough in. 527 

partial or complete loss of voice in, 

527 
short, sharp, brassy cough in, 527 
whispering voice in, 557 
Laveran, malarial germ of, 396 
Lead colic, retraction of abdominal 
wall in, 281 
epilepsy, 496 

chronic paralysis in, 46 
gait in, 60 

peripheral neuritis in, 181 
poisoning, blue line on gums in, 124 
tremors in, 49 
Leg, milk, 93 

paralysis of, 88 
Legs, feet and, 59 

deformities of, 88 
swelling of, 93 
Leprosy, appearance of hands in, 39 
gangrene in, 39 
hyperesthesia in, 189 
leonine face of, 16 
Leptomeningitis, diagnosis of coma in 
purulent, 489 



590 



INDEX 



Leptomeningitis, hyperesthesia in 

chronic, 189 
Leukocytes, 374 

differentiation of, 382 
mononuclear, 383 
polynuclear, 383 
transitional, 383 
Leukocythemia. See Leukemia. 
Leukocytosis, 393 
digestion, 393 
gravid, 393 
in acute diseases, 395 
in appendicitis, 395 
in cholangitis, 457 
in intestinal obstruction, 396 
in pneumonia and other infectious 

diseases, 395 
in trichiniasis, 396 
iodophilia in, 396 
terminal, 396 
Leukoderma in goitre, 138 
Leukokeratosis buccalis, 119 
Leukoma of tongue, 119 
Leukopenia, 396 
Leukemia, hematuria in, 338 
lymphatic, 395 
splenomedullary, blood in, 394 

enlargement of spleen in, 310, 
395 
uric acid in urine in, 351 
Lichen planus, tongue in, 120 

ruber, nails in, 35 
Lienteric diarrhea, 318 
Light, pupillary, reaction to, 426 
Lineae albicantes, 280 
Lingual paralysis, 121 

ulcers, 118 
Lips, blueness of, in heart disease, 258 
fulness of, in persons of strong sexual 
appetite, 10 
indicating phlegmatic tempera- 
ment, 10 
greatly thickened in cretinism, 15 
immobility of, due to mucous 
patches or ulceration of buccal 
mucous membrane, 12 
pendulous, in progressive bulbar par- 
alysis, 25 
slightly parted, dry, and cyanotic in 
chronic pulmonary or cardiac dis- 
ease, 13 
thin and mobile, in nervous indi- 
viduals, 10 
twitching of raised upper, in peri- 
tonitis or pain below diaphragm, 
13 
Lithemia, cylindroids in urine in, 348 
Litten's sign, 203 

Liver, acute yellow atrophy of. See 
Yellow atrophy, acute, 
amyloid disease of, jaundice in, 133 
causes of tenderness of, 302 



Liver, cirrhosis of, hematemesis in, 518 
jaundice in, 132 
enlargement of, 285 

position in, 4 
floating, 303 
hematemesis in, 518 
headache in congestion of, 470 
hydatid cyst of, 304 
indicanuria in cancer of, 341 
jaundice in, 133 

malignant disease of, jaundice in, 
132 
nodules and umbilication of, in, 
301 
percussion note over, 210, 300 
pushed down bv right-sided pleural 

effusion, 301, 303 
rough, in cirrhosis, 301 
swelling of, in Weil's disease, 460 
symptoms of cirrhosis of, 301, 302 
of malignant disease of, 301 
of tropical abscess of, 303 
vomiting in, 522 
Localization of functions of segments of 

spinal cord, 79, 82 
Localized sweating, 161 
Locomotor ataxia, 59 
allochiria in, 187 
analgesia in, 173 
anesthesia of lower portion of body 

and of legs in, 173 
Argyll-Robertson pupil in, 60, 427 
athetoid movements in, 52- 
bladder symptoms of, 331 
blunted and delayed sensation in, 

173 
brachial monoplegia in, 54 
cardiac feebleness in, 264 
coffee-ground vomit in gastric 

crisis of, 517 
contracted pupil in, 428 
cutaneous hemorrhages in, 142 
diagnosis of, 553 

from Friedreich's ataxia, 63 

from general paresis, 163 

from hereditary cerebellarataxia, 

64 
from hysteria, 62 
diarrhea as an intestinal crisis of, 

318 
dilatation of pupil in, 428 
diplopia in, 413 
double sciatic pain in, 539, 542, 

548 
flatfoot in, 89 
gait of, 59 

gastric crisis of, 60, 517 
girdle sensation in, 188 
hematuria in, 338 
hemiplegia in, 109 
hyperesthesia in, 188 
hypotonus in, 61 



INDEX 



591 



Locomotor ataxia, inability to use fin- 
gers and hands in, 51 
joints in, 90 
intestinal crisis in, 318 
laryngeal crisis of, 60 

spasm in, 242 
lesion of optic nerve in, 440 
loss of knee-jerk in, 60, 553 
mu cular atrophy of arm in, 54 

hypotonus in, 61 
numbness of feet in, 60 
nystagmus in advanced, 425 
ocular symptoms of, 440 
optic atrophv in, 440 
pain in, 539, 642, 548 

of skin in, 190 
paraplegia in, 83, 75 
paresthesia in, 186 
perforating ulcer in, 95, 158 
ptosis in, 24, 413 
retention of urine in, 331 
Romberg's symptom of, 60 
swaying of body in, 60 
syphilis a frequent cause of, 59 
thoracic pain in, 540 
tongue in, 120 
twitching of fingers in, 51 
vesical crisis of, 60 
Westphal's sign of, 60 
Lordosis in cretinism, 16 

in progressive muscular atrophy, 43 
Lumbago, pain in, 541 
Lumbar puncture, 462 

in diagnosis of cerebrospinal men- 
ingitis, 462 
of tuberculous meningitis, 478 
Lupus, ulceration of tongue in, 118 
Lymphangioma, congenital, tongue in, 

120 
Lymphatic leukemia, 395 
Lymphocytes, 383 

Lyons' method of estimating urea, 366 
Lysis, fever in erysipelas, ending by 
crisis or, 455 
in scarlet fever, ending by, 453 
in smallpox, ending by, 454 
in typhoid, ending by, 447 
in catarrhal pneumonia, 465 
rare in croupous pneumonia, 464 



M 

McBurxey's point, 546 
Microglossia, 120 
Macrocvtes, 385 
Macula lutea, 438 
Maddox-rod test, 415 
Madura foot, 40, 95 
Main en griffe, 40 
Malaria, anemia in, 391 
aortitis rare «n. 540 



Malaria, blood in, 396 
brow ague in, 537 
Cheyne-Stokes breathing in hema 

turic, 201 
chill in, 442 
coma in, 4s , 
convulsions due to, 497 
diazo-reaction in, 370 
enlargement of spleen in, 310 
examining organism of, 403 
glycosuria in convalescence from, 

364 
headache in, 482 
hematemesis rare in. 518 
hematuria in, 335. 336 
hemoglobinuria in, 340 
intermittent, attacks occurring ear- 
lier each day in. 456 
characteristic of lexer, quartan, 
456 
quotidian, 456 
tertian. 456 
chill, fever, and sweats in, 155 
diagnosis of, 156 
effect of quinine on. 156 
parasite of estivo-autunmal, 398 
of quartan. 398 
of tertian. 307 
pernicious, differential diagnosis be- 
tween yellow fever and, 4 * > 1 
remittent, bilious vomiting in. 459 
character of lexer in. 45!) 
diagnosis between typhoid fever 
~ and, 449 
between yellow lever and. 460 
due to estivo-autunmal parasite, 

459 
jaundice in, 459 
sweating in, 161 
synonyms of. 459 
retinal hemorrhage in. 441 
roseola in, 148 
splenic enlargement in. 310 
skin in, 136 

staining organisms of, 400 
sweating in. 161 
Malarial germ of Laveran, 396 
organisms. 396 

Xocht's modification of Roman- 
owsky's stain for, 400 
Malignant pustule. Sec Anthrax, ma- 
lignant. 
Malingering, convulsions in, 502 

inability to ape facies of disease in. 10 
merycismus in, 523 
sciatica in. 542 
Malta fever, anorexia in. 452 
character of fever in. 452 
frequency of relapse in, 452 
headache in. 452 
insomnia in. 452 
pain on motion in, 452 



592 



INDEX 



Mammary gland, enlargement of, in 

pulmonary tuberculosis, 199 
Mania, acute, dilatation of pupil in, 428 
Maniacal chorea, 47 
Marasmus, sinking in of fontanelle in, 

32 
Measles, character of fever in, 454 
date of eruption in, 147 
diazo-reaction in urine of severe, 370 
headache in, 482 
rash of, 146 

on pharynx and buccal mucous 

membrane, 128 
symptoms of, 146 
Meckel's diverticulum, 514 
Mediastinal abscess, diagnosis of, from 
mediastinal tumors, 243 
growths, cause of laryngeal spasm, 
242 
bulging of chest in, 198 
caput Medusae in, 285 
diagnosis of, from abscess, 243 
from aneurysm, 243 
from chronic pneumonia, 243 
from pericarditis, 243 
from pleural effusion, 243 
dysphagia in, 124 
hoarseness of voice due to pressure 

by, 557 
laryngeal cough due to pressure on 

larynx by, 527 
pain in, 540 

signs and symptoms of, 242 
Mediastinopericarditis, indurative, pul- 
sus paradoxus in, 274 
epigastric pulsation in, 204 
hiccough in, 508 
Megaloblasts in pernicious anemia, 392 
Megalocytes, 385 
Megrim. See Migraine. 
Melancholia, facial expression in, 14 
puerperal lingual spasm in, 123 
with oxaluria, diagnosis of, 351 
Melanotic cancer, black urine in, 335 
Melena neonatorum, vomiting in, 518 
Meniere's disease, symptoms of, 483 
vomiting following tinnitus au- 
rium and vertigo in, 522 
Meningeal irritation, tache cerebrale in, 
144 
tuberculosis, Cheyne-Stokes respira- 
tion in, 201 
Meningitis, basilar, lesions causing ocu- 
lar paralysis in, 419 
papillitis in, 439 
retraction of head in, 30 
bilateral anesthesia in, 173 

loss of knee-jerk, 553 
bulging fontanelle in purulent, 31 
cerebrospinal. See Cerebrospinal 

meningitis, 
contracted pupil in, 412 



Meningitis, contraction of hand in, 45 

diplopia in, 413 

facial spasm in, 27, 28 

hippus in acute, 429 

hyperesthesia in cerebrospinal, 188 

Kernig's sign, 479 

lumbar puncture, 462 

nystagmus, 425 

occipital headache in, 510 

pain in nape of neck in, 510 

piercing cry in, 7 

pseudo-, 503 

purulent, hemiplegia in, 110 
vomiting in, 510 

reflexes in, 553 

retraction of head in, 30 

rigidity of dorsal muscles in, 510 

scaphoid belly in tuberculous, 281 

spinal, dilatation of pupil in, 428 
loss of knee-jerk in, 553 

subnormal temperature in, 467 

symptoms of, 474, 475, 476 

tache cerebrale in, 144 

tuberculous, 476 
papillitis in, 439 
reflexes in, 555 

vomiting in, 510 
Menstruation, anemia due to profuse, 
391 

dark areas under eyes during, 10 

disorders of, in chlorosis, 393 

hematemesis as vicarious, 518 

hemoptysis as vicarious, 529 
Merycismus, 523 

Mesenteric glands, tuberculosis of, 294 
Mesentery, cysts of, 309 
Metallic tinkling heard over chest in 
cavity, 222 
over hydropneumothorax, 222, 

235 
over stomach, 223 
in pleural effusion with pneumo- 
thorax, 235 
Metatarsal neuralgia, 550 
Methylene-blue test to determine ac- 
tivity of kidneys, 344 
Microcephalus, 30 
Microcytes, 385 
Microorganism of influenza, cause of 

empyema, 239 
Migraine, hemianopsia in, 469 

hyperesthesia in, 189 

muscse volitantes in, 436 

scotomata in, 523 

sweating of head in, 161 

symptoms of, 538 

vomiting in, 522 
Miliaria, 161 
Milk leg, joints in, 93 
Milky-looking urine, 339, 340 
Mirror writing, 52 
Mitral disease, 247 



INDEX 



:m 



Mitral obstruction, 249 

and regurgitation, accentuation of 
pulmonary second heart sound 

in, 2 IS 
regurgitation, 247 

precordial tin-ill in, 2 is 
pulse in, 273 
symptoms of, 258 
stenosis, gallop rhythm in, 241) 
pulse in, 273 
reduplication of heart sounds in, 

246 
thrills in, 207 
Moebius' sign, 112 
Moist rales, 222 
Moller- Harlow's disease, 01 
Mono-anesthesia, 171 
Mononuclear leukocytes, 383 
Monoplegia, 52, 86 
brachial, 52 

bilateral, 55 
of lower extremities, 86 
spastic, 7 I 
Morbilli, 146. See Measles. 
Morphine as a cause of facial hemi- 
atrophy, 17 
Morton's painful toe, 550 
Monad's disease, 13 

gangrene of hands in, 39 
small joints affected in, 89 
Mosquito as a carrier of malarial para- 
sites, 401 
development of, 101 
Mouth breathers, 12 
in heart disease, 12 
in paralysis of salivary glands, 12 
nasal twang of voice in, 558 
pigmentation of, 264 
Mowing gait, 68 

Mucomembranous enteritis, 318 
Mucous disease, tongue in, 115 
membrane, buccal, 126 
patches about mouth and anus in 
infantile syphilis, 12 
immobility of lips due to, 12 
Multiple sclerosis. See Sclerosis, dis- 
seminated. 
Mumps, enlarged parotid glands in, 33 

peptonuria in, 360 
Murmur, anemic, 246 
in enteritis, 246 
aortic regurgitant, 250 

capillary pulsation in, 259 

Corrigan's pulse in, 250, 259 

dyspnea in, 259 

ox-heart in, 250 

pulsation of retinal arteries in, 

259 
Quincke's sign of, 259 
short and sharp pulse in, 373 
w'ater-hammer pulse in, 250, 259 
stenosis, 250 

38 



Murmur, aortic stenosis, small and hard 
pulse in, 373 
symptoms of, due to failing com- 
pensation, 259 
cardiopulmonary, 210 
heart, 240 

hemic, over fontanelle in rick< 
humming-top, in jugular vein in 

chlorosis. 393 
in splenic leukemia, 395 
mitral regurgitation, 247 

small volume of pulse in, 373 
symptoms of, clue to failing 

compensation, 258 
thrill in, 248 
stenosis, 249 

gallop rhythm in, 249 
pulse wave of. 275 
small volume of pulse in, 273 
symptoms of, due to failing com- 
" pensation, 250, 259 
thrill in, 249 
pulmonary regurgitation, 255 
stenosis, 255 
valvular, 255 
tricuspid regurgitation. 255 
stenosis, 255 

systolic, in emphysema, 240 
Musca? volitantes, 436 
Muscle tone, 552 

Muscles, contraction of. in paramyo- 
clonus multiplex, 17 
in electric chorea of Bergeron, is 
in Huntingdon's chorea, 18 
in "jumpers," 48 
intra-ocular. 425 

shock-like, in Dubini's disease. 18 
ocular, paralysis of, 413 
Muscular atrophy, faciohumeroscapular 
type of, 14 
hands in, 36 

idiopathic. See Atrophy, idio- 
pathic muscular, 
progressive, clawhands in, 42 
diagnosis of, from Friedreich's 
ataxia, 75 
from multiple neuritis, 75 
from poliomyelitis, 75 
reflexes in, 555 
spastic monoplegia in, 74 
Murism, hysterical, 557 
Myalgia, pain in, 541, 542 
Mycetoma, 40, 95 
Mycoses, appearance of tongue due to 

growth of, 115 
Mydriasis, irritative, 428 

paralytic, 428 
Myelitis, acute, ascending, 77, 158 
central, 76 
disseminated, 65 
transverse, allochiria in, 187 
anesthesia in, 173 



594 



INDEX 



Myelitis, acute, transverse, bed-sores 
in, 58 
bilateral anesthesia in, 174 
bladder, symptoms of, 77, 330 
collateral symptoms, 331 
diagnosis of cervical, dorsal, and 

lumbar, 79, 80, 81 
effect of lesion in, 77 
girdle sensation in, 74, 188 
hyperesthesia in, 188 
knee-jerk in, 553, 554 
non-spastic, anesthesia in, 77 
bed-sores in, 77 
girdle sensation in, 77 
•paraplegia in, 77 
reflexion in, 77 
paresthesia in, 187 
sensory paralysis in, 74 
spastic paraplegia in, 74 
symptoms of, 77 
chronic, gait of, 65 

transverse, differential diagnosis 
of lumbar, dorsal, and cervical, 
79 
hemilateral, 86 
hiccough in, 508 
subacute, 77 
transverse, 77 

traumatic, retention of urine in, 330 
Myelocyte, 383 

of Ehrlich, in splenomedullary leu- 
kemia, 394 
Myelopathic albumosuria, 360 
Myocarditis, degenerative, 264 
Myoclonus multiplex, 47 
Myosis in facial hemiatrophy, 16 
irritative, 428 
paralytic, 428 
Myotonia congenita, 48, 507 
Myxedema, diagnosis between dropsy 
and, 143 
enlargement of feet in, 88 

of tongue in, 121 
face of, 15 
head in, 30 
skin in, 138 
spade-like hand in, 40 
symptoms of, 143 



N 



Nails, atrophy of, 35 
hypertrophy of, 35 
in acute fevers, 35 
in anemia, 34 
in chloral habit, 35 
in eczema, 35 
in gout, 35 
in hemiplegia, 35 
in lichen ruber, 35 
in prolonged illness, 35 



Nails in psoriasis, 35 

in pulmonary osteoarthropathy, 35 

in Raynaud's disease, 35 

in sclerodactyle, 35 

in syphilis, 35 

in syringomyelia, injury, or neuritis, 

35 
infantile palsy, 35 
white spots on, 35 
Nasal catarrh, chronic atrophic, breath 
in, 3 
headache in, 482 
obstruction, facial expression in, 12 
Nausea, acute, position in, 4 
Necator americana, 327 
Neck, spasm of muscles of, 29 
Necrosis, anemic, 264 

fat, from impacted gallstone, 304 
Nephritis. See also Kidneys and 
Bright's disease, 
acute, 317 
diffuse, 371 

hemorrhagic effusions in, 238 
irritation of bladder in, 332 
parenchymatous decrease of urine 
in, 334 
epithelial casts in urine a posi- 
tive sign of, 345 
chronic hemorrhagic, 335 

interstitial, 350, 372, 373, 374 
parenchymatous, 334, 372 
skin in, 138 > 
Nervous bladder, 333 
diarrhea, acute, 317 
exhaustion, headache in, 471 
Neuralgia, causes of, 537 

due to lead or arsenic poisoning, 537 

due to malaria, 537 

edema in, 164 

hyperesthesia in, 189 

intercostal, 540 

metatarsal, 550 

Morton's painful toe in, 550 

occipital, 539 

of fifth nerve, infra-orbital, 538 

of foot, 550 

of head, 537 

of labia majora or perineum, 541 

of pelvic viscera in women, 541 

pain in, 537 
sciatic, pain in, 541 
supra-orbital, diagnosis of, from neu- 
ritis, 537 
Neurasthenia, gait in, 2 
headache in, 471 
hyperesthesia in, 188 
increase in urine in, 334 
intestinal sand in, 324 
knee-jerk increased in, 554 
paresthesia in, 187 
scapulohumeral reflex in, 552 
vomiting in, 520 



INDEX 



595 



Neuritis, acute multiple, fever in, 466 
knee-jerk lost in, 553 
symptoms and signs of, 466 
arsenical, gait in, 60 
cause of anesthesia, 180 
diagnosis of, 553 
diphtheritic, 182 
in foot, leg, and thigh, distribution 

of anesthesia in, 185 
in hand, distribution of anesthesia 

in, 184 
multiple, 466 

optic, 438. See Papillitis, 
peripheral anesthesia in, 181 
clawhand in, 41 
general anasarca in, 163 
hyperesthesia in, 188 
nails in, 35 
skin in, 157 
retrobulbar, 431) 
sciatic, diagnosis of, 541, 542 
knee-jerk in, 553, 554 
limping gait of, 59 
pain in, 541 
tender joints in, 542 
toxic peripheral, 181 
Neuroma, pain in, 550 
Neurosis, cardiac, 263 
Neutrophile corpuscles, 383 
Newborn, cyanosis in, 138, 139 
edema in, 144 
jaundice in, 135 
sclerema in, 144 
Nictitating spasm, 27 
Nitric acid test for albumin, 356 
Nocht's modification of Romanowsky's 

stain for malarial parasites, 400 
Nodding spasm, 28 
Noma, 126 
Normoblasts, 385 

Nose, anemia due to hemorrhage from, 
391 
asthma due to reflex irritation in, 241 
broad and flat, in cretinism, 15 
broadness of bridge of, an indication 

of congenital syphilis, 12 
dilated, in heart disease, 12 
hemorrhage from, in leukemia, 395 
in mouth breathers, 12 
pinched and drawn, indicating pain 
in chest in children, 12 
Nystagmus, 425 

in acute meningitis, 425 
in children, 425 

n disseminated sclerosis, 64, 425 
in epilepsy, 425 
in Friedreich's ataxia, 63, 425 
in growths in cerebellum or pons, 425 
in hydrocephalus, 425 
in locomotor ataxia, advanced, 425 
in multiple sclerosis, 425 
in spastic paraplegia, 71 



Obermeier, spirillum of, 453 
Obesity, urine in, 363 
Obstructive jaundice, 131 
Occult blood in stools, test for, 323 
Occupation spasm, 46 
Ochronosis, skin in, 136 
Ocular muscles, paralysis of, 413 
Oculofacial paralysis, 26 
Oculomotor paralysis, 421 
Oligochromemia, 389 
Oligocythemia, 374 
Omentum, tuberculosis of, 294 

tumors of, 294 
Onychogyrophosis, 35 
Ophthalmoplegia, 22 
Ophthalmoscopy, 436 
Opisthotonos in hysteria, 499 

in severe meningitis, 510 
Opium poisoning, 485 

differential diagnosis between poison- 
ing from alcohol and, 485 
Oppenheimer's modification of Den- 

nige's test for acetone in urine, 365 
Opsonic index, 408 
Optic atrophy, 440 

neuritis, 438 
Orthophoria, 415 
Orthostatic albuminuria, 359 
Osteitis deformans, head in, 30 

of cranial bones, headache in, 482 
triangular face of, 17 
Osteomalacia, gait of, 68 
Osteomyelitis, acute, arthritis in, 91 

joint involvement with fever, 466 
Osteophytes, formation of, in rheuma- 
toid arthritis, 90 
Otitis in scarlet fever, 453 

media, with thrombosis of cavernous 
sinus, 480 
diagnosis between cerebrospinal 
meningitis and, 462 

vertigo in, 483 
Ovarian cysts, 281 

Oxaluria, concomitant symptom of mel- 
ancholia, 351 

cylindroids in urine of, 349 

due to ingestion of pears, cabbage, 
and tomatoes, 351 

spermatorrhea in, 351 

yellow color of skin in, 136 
"Ox-heart" of aortic regurgitation, 250 
Oxyuris vermicularis, 327 
Ozena, breath in, 3 



Pachymeningitis interna hemorrhag- 
ica, coma in, 489 
headache in, 480 



596 



INDEX 



Pachymeningitis, spinal, spastic para- 
plegia in, 72 
Pain, abdominal, 542 

below diaphragm, twitching of upper 

lip in, 13 
bilateral, of rheumatism of scalp, 

538 
burning, in esophagus, stomach, and 

abdomen in phosphorus poisoning, 

521 
causes of circumscribed abdominal, 
548 

in neighborhood of heart, 539 

in sacral region, 541 

neuralgic, 537 

sciatic, 541 

supra-orbital neuralgic, 537 
colicky, extending to right shoulder 

in acute pancreatitis, 521 
concomitant symptoms of abdom- 
inal, 7 
crisis of, in tabes, 60 
darting, in urethra, in cystitis, 331 
distribution of, in neuralgia of fifth 

nerve, 537 
expression about eyes in children 
due to, 11 
of face due to, II 
in abdominal colic, 512 
in acute aortitis, 539 
in aneurysm, 254, bib 
in angina pectoris, 539, 540 
in angioneurotic edema, 545 
in appendicitis, 289, 513 
in back, causes of, 551 
in bellyache, 4 

in carcinoma of caput coli, 543 
in cardiac disease in children, 6 
in cerebral tumor or abscess, 539 
in chest in aortic aneurysm, 540 
in cholecystitis, 543 
in cholelithiasis, 544 
in coxalgia, 6, 541 
in cystitis, 550 
in dengue, 551 
in diabetes mellitus, 549 
in diarrhea, 6 
in diffuse hepatitis, 544 
in dysentery, 319 
in dysmenorrhea, 550 
in dyspepsia, 541 
in enterocolitis, 318 
in fecal impaction, 547 
in fissure of the anus, 550 
in floating kidney, 306, 547 
in gallstone colic, 543 
in gastralgia, 549 
in gastric cancer and ulcer, 290, 291, 

541, 544 
in head in children, 11 
in hemoglobinuria, 522 
in hemorrhagic infarction, 515 



Pain in hepatic colic, 543 
in hepatitis, 544 
in hip disease, 541 
in intercostal neuralgia, 539, 540 
in intestinal indigestion, 544 

obstruction, 510, 512, 547 

perforation, 304, 546 
in intussusception, 511, 512 
in jaundice due to gallstones, 131 
in lead colic, 547 

in locomotor ataxia, 539, 542, 548 
in lumbar region due to perineph- 
ritic disease, 342 
due to pyelitis, 342 
due to stone in kidney or ureter, 
342 
in malignant growth of femur, 542 
in mediastinal growths, 540 
in meningeal hemorrhage, 480 
in migraine, 538 
in neuralgia of foot, 550 
of head, 537 
of pelvic viscera, 541 
in neuritis, 537, 5 . 1 
in neuromas, 550 
in occipital neuralgia, 538 
in one side of head in migraine, 538 
in pancreatic calculus, 544 
in pancreatitis, 546 
in pelvic growths, 541 
in pericarditis, 540, 541 
in peritonitis, 546 
in pleuritis, 540 

in pseudo-angina pectoris, 539, 540 
in pulmonary diseases in children, 6 
in pyelitis, 342 
in renal calculus, 542 

colic, 547 
in rheumatism of scalp, 538 
in rickets, 541 
in sciatic neuralgia, 541 
in scurvy, 541 
in skin in tabes dorsalis or hysteria, 

190 
in spinal caries, 541 
in syphilitic periostitis of skull, 538 
in typhoid fever, 546 
often referred to point distant from 

its source, 537 
sense, 165, 166 
summary of conditions producing 

acute, sudden, 549 
tearing, burning, in hemorrhage into 

membranes of cord, 174 
thoracic, in locomotor ataxia, 540 
throbbing, in inflammation, 536, 550 
varieties of, 536 
Palmus, 48 
Palsy, cerebral, of children, 44 

increased knee-jerk in, 554 
crutch, 46 
infantile, acute, nails in, 35 



INDEX 



597 



Pancreas, abscess of, 305 
carcinoma of, 294 
cysts of, 304 

fatty diarrhea due to disease of, 321 
hemorrhagic inflammation of, 304 
inflammal ion of, 304 

pain in, 546 

symptoms of, 521, 546 

vomiting in, 521 
jaundice in disease of, 133 
Pancreatic calculi in stools, 324 
calculus, pain in, 546 
carcinoma, 294 
cysts, 301 
diabetes, 294 
Pancreatitis, acute hemorrhagic, 304 

vomiting in, 521 
malignant, 304 
Papillitis, 438 

in acute febrile disorders, 439 
in anemia, 439 

in brain tumor, 439, 472, 509 
in cerebral abscess, 439 
in meningitis, 439 

tuberculous, 439 
in rheumatism, 439 
in syphilis, 439 
in toxemia From alcohol, 13!) 

from lend, 439 
Papilloma of bladder, hematuria due 

to, 338 
Paresthesia, 186. Sec also Allochiria. 
brachial, 56 

from exposure to carbolic acid. 1ST 
in aconite poisoning, 1ST 
in brain tumor, IS? 
in carbolic acid poisoning, 1ST 
in locomotor ataxia, 186 
in myelitis, 187 
in neurasthenia, 1ST 
in spinal syphilis, 186 
Paralysis agitans, allochiria in. 187 

festination in, 505 

gait in, 67 

hands in, 44 

Parkinsonian visage in, 14, 505 

speech and voice in, 559 

tremor of hands in. 44, 49 
asthenic, bulbar. 20 

diagnosis between progressive bul- 
bar paralysis and. 20 

speech of, 559 
bilateral facial, 25 
bulbar, acute, 25 

ophthalmoplegia in, 419 

asthenic, 26 

progressive, 25 
cerebral, acute, infantile, causing 
hemiplegia, 109 

deformity of foot in acute, 75 

diagnosis between paralysis of leg 
in. and poliomyelitis. 73 



Paralysis, cerebral, diagnosis between 
hereditary spast 1c paralysis 
and, 73 
hysteria and, 73 
spinal paralysis and. 73 

epileptic convulsions in. 73 

gait of infantile, 66 

mirror writing in, 52 

movements of hand in. 51 

spastic paraplegia in. 70 
crossed, 20, 110 
diphtheritic, 25 

dysphagia in, 124, 125 

knee-jerk in. 553 
due to myelitis, 76, 77 

to tumor of brain, 473 
Erb's, 55 

family periodic, 85 
glossolabiopharvngeal, 25 

bilateral atrophy of tongue in, 120 
facial paralysis due to, 25 

biting the tongue in, 119 

cardiac feebleness in. 204 

cough in. 527 

diagnosis of, 559 

dysphagia in, 124 

fibrillary tremor of tongue in, 123 

indistinct speech of mumbling 
character in, 559 

movements of tongue in, 121 

reflexes in, 555 
hereditary spastic, 73 
hysterical, 68 
infantile spinal. See Poliomyelitis, 

anterior. 
Klumpke's, 55 
laryngeal, causes of, 558 
oculofacial, 20 
of bladder with retention, due to 

pressure during childbirth. 330 
of insane, progressive, eyes in, 428 
of intra-ocular muscles. 425 
of muscles of jaw, 22 

of leg, 87 
of ocular muscles, 413 
of one arm, 52 
of salivary glands, causing dryness 

of mouth, 18 
of tongue, 121 
progressive bulbar, 25 
pseudobulbar, tongue in, 121 
recurrent, of oculomotor nerve of one 

side, 25 
reflex, 84 

sometimes found instead of occupa- 
tion spasm, 46 
unilateral facial, 18 
Paralytic chorea, 47 
mydriasis, 428 
myosis, 428 
squint, 414 
Paramyoclonus multiplex, 47 



598 



INDEX 



Paramyoclonus multiplex, diagnosis 

of, 506 
Paramyotonia congenita, 48 
Paraphasia, 560 
Paraplegia, 69 
ataxic, 66, 83 

knee-jerk exaggerated in, 554 
non-spastic, 75, 76, 77 
of rickets, 71 
reflex, 84 

spastic, cerebral, 69 
spinal lesions causing, 69, 72 
Parasites, anemia due to Ankylosto- 
mum duodmale, 328, 391 
due to tape-worm, 328, 391 
intestinal, Ankylostomum duodenale, 
327 
Ascaris lumbricoides,, 327 
Bothriocephalus latus, 327 
Oxyuris vermicularis, 327 
Tenia cucumerina, 327 
mediocanellata, 326 
solium, 326 
Trichocephalus dispar, 328 
Uncinaria americana, 327 
of blood, 396 
of lung, Distoma pulmonum, 533 

echinococcus, 533 
of malaria, estivo-autumnal, 398 
quartan, 398 
tertian, 397 
of urine, Distoma hematobium, 338 
Filaria sanguinis hominis, 403 
Paravertebral triangle of dulness of 

pleural effusion, 234 
Paresis, delusions of grandeur in, 331 
cyanosis in, 139 
diagnosis of coma of, 490 
diplopia a symptom of, 413 
fine intention tremor in, 63 
gait of, 63 
hemiplegia in, 110 
Jacksonian epilepsy in, 493 
spasm of tongue in, 123 
tremor of hands in, 50 
vesical symptoms of, 331 
Paretic dementia, bilateral atrophy of 
tongue in, 120 
cyanosis in, 139 
greasy, yellow skin in, 136 
hemiplegia in, 110 
hemorrhages into skin in, 142 
localized sweating in, 161 
optic atrophy in, 440 
perforating ulcer of foot in, 158 
speech in, 559 
tache cerebrale in, 144 
vesical symptoms of, 331 
Parkinson's disease, 49 
Parkinsonian visage, 14, 505 
Paronychia, 35 
Parotitis in pyemic fever, 33 / 



Parotitis in typhoid fever, 33 

in typhus fever, 33 
Parrot tongue, 116 
Patellar reflex, 552 
Pectoriloquy in tuberculosis, 230 

over cavity connected with a bron- 
chial tube, 226 
Pediculi, pigmentation of skin in, 137 
Peliosis rheumatica, 140. See Purpura. 
Pemphigus, eruption of, 157 
Peptonuria, 360 
Pentosuria, test for, 364 
Percussion, direct, 207 

note, coin test in hydropneumotho- 
rax, 235 
cracked-pot sound, 211, 212 
dull, in consolidation of lung in 
pneumonia, 211 
in pulmonary congestion, 232 
edema, 232 
flat, over liver, 210, 300 

pleural effusion, 210, 232 
tympanitic, in lung, due to collapse 
or adhesion of lung, 212 
to consolidation, 211 
to large cavity, 211 
to pneumothorax, 211 
of heart and great vessels, 213 
of respiratory organs, 210 
resonance, cause of, 208 
trimanual, 309 
Perforating ulcer of foot, 95 
Pericardial friction sounds, 257 
Pericarditis, adhesive, 302 
pain in, 540, 541 

with effusion, diagnosis of, from car- 
diac dilatation, 216 
from hypertrophy, 216 
from mediastinal tumors, 243 
bulging of chest in, 196 
displaced apex beat in, 205 
signs and symptoms of, 215 
Pericardium, adherent, 204 
Perimeter, 432 
Perinephritic abscess, 309 
Periosteal thickening of bones of leg, 

95 
Peristaltic waves, 281 
Peritonitis, acute, symptoms of, 288, 
304, 546 
tongue in, 116 
expression of anxiety in, 11, 13 
fever in, 516 
hiccough in, 508 
indicanuria in, 341 
muscular rigidity in, 288 
pain in, 288, 546 
position of body and head in, 4 
pulse in, 273 

small, wiry, 273 
tuberculous, erythema in, 150 
tympanites in, 281 



INDEX 



599 



Peritonitis, vomiting in, 516, 523 
Peroneal leg type of progressive mus- 
cular atrophy, 75 
Pes equinus, 74 
Petechia? from drugs, 142 

in acute ulcerative endocarditis, 142 

in cerebrospinal meningitis, 142 

in scurvy, 142 

in septicemia, 142 

in snake-bite, 142 

in typhus fever, 149, 452 

in wasting, 142 
Petit mal. See Epilepsy, minor. 
Phantom tumor of abdomen, 309 
Pharyngitis associated with stomach 
cough, 528 

dysphagia due to, 124, 125 

simple acute, 127 
Phenylhydrazin test for sugar in urine, 

363 
Phlebitis, fever in, 457 
Phlegmasia alba dolens, 164 

edema in, 164 
Phloroglucin-vanillin test, 299 
Phosphaturia, cloudy urine in, 350, 
352 

headache associated with, 471 
Phthiriasis versicolor, skin in, 137 
Phthisis. See also Tuberculosis. 

alar chest of, 194 

cause of night cough in, 527 

character of cough in laryngeal, 526 
of sputum in, 530 

"cog-wheel" breathing an early sign 
of, 220 

expansion of chest in, 230 

facial expression in, 12 

fibroid, physical signs in, 230 

flushing of face in, 142 

greasy, yellow skin in, 136 

hands in, 34 

laryngeal, whispering voice in, 557 

night sweats of, 161 

pneumonic, acute, 230 

tongue in advanced, 116 

vomiting in, 523 
Pigeon breast, 198 

Pigmentation of eyelids in pregnancy, 
10 

of skin, 136 
Piles. See Hemorrhoids. 
Plantar reflex, 555 

Pleural effusion. See Effusion, pleural. 
Pleurisy, acute, chest expansion in, 202 
friction sound in, 223, 232 
pain in, 6, 540 
symptoms and signs of, 232 
tenderness over rib in, 189 

hemorrhagic, 238 

interlobular, physical signs of, 238 

with effusion, 232 
apex beat in, 206 



Pleurisy with effusion, Baccelli's sign 
above, 225 
bronchial breathing due to com- 
pression in, 220 
bulging of chest in, 195, 232 
changes in level of effusion in, 233 
chest expansion in, 202 
convulsions during irrigation of 

pleura in, 503 
cough during aspiration of fluid 
in, 527 
on change of position in, 527 
cracked-pot sound in, 211, 212 
distant breath sounds over effu- 
sion in, 234 
edema over ribs in purulent, 164 
egophony above effusion in, 226, 

234 
Litten's sign of, 203 
method of testing for cause of, 236 
of left side, obliteration of 
Traube's semilunar space 
in, 234 
spleen displaced downward 
in, 311 
of right side, liver pushed down in, 

301, 303 
position in, 4 
pulsating, 207 

sigmoid line marking top of effu- 
sion in, 234 
skodaic resonance above effusion 

in, 212, 234 
symptoms and signs of, 232 - 234 
vocal fremitus in, 205 
resonance in, 225 
Pleuritis. See Pleurisy. 
Plumbic gout, 92 
Pneumococcus as a cause of empyema, 

239 
Pneumonia, acute catarrhal, difficulty 
of diagnosis between pulmo- 
nary tuberculosis and, 227, 
229 
fever in, 465 
physical signs of, 229 
puerile breathing in, 220 
symptoms and signs of, 226 
croupous, casts of finer bronchial 
tubes sometimes found in spu- 
tum of, 531 
fever in, 464 
bronchial breathing in, 226 
bubbling rales in resolution in, 222 
Cheyne-Stokes respiration in, 201 
chill in, 442, 464 
chlorides decreased in urine in, 370 

increased in, 370 
chronic Charcot-Leyden crystals in 

sputum of, 531 
cracked-pot sound in, 212 
crepitant rale an early sign of, 222 



600 



INDEX 



Pneumonia, crisis in, 226, 464 

croupous, diazo-reaction in, 370 
peptonuria in, 360 

crying in children with, 6 

Curschmann's spirals in sputum of, 
530 

delirium in, 227 

diagnosis and symptoms of, 226 
between mediastinal growths and, 
243 
pneumonic phthisis and, 227 

dilatation of pupil in, 428 

expansion of chest in, 203 

expression of anxiety in, 11 

face of, 12 

feeble heart in, 227 

headache in early stages of, 481 

herpetic blisters about mouth, with 
fever in, 12, 155, 226 

increase in urine in convalescence 
from, 334 
of vocal fremitus in, 205 
resonance in, 225 

jaundice in, 135 

leukocytosis in, 395 

necessity for examining axilla and 
septum between upper and middle 
lobe of right lung in, 227 

percussion note dull in, 211, 227 

prune-juice or purulent sputum . in, 
227, 529 

pseudocrisis in, 227, 464 

rale redux in, 227 

rapidity of respiration in, 200 

rusty, sticky sputum in, 226, 528, 
529 

secondary diphtheritic dysentery due 
to, 320 

subnormal temperature following 
crisis of, 464, 467 

sweat at crisis in, 160 

vocal resonance in, 225 

wavy breathing of, 203 
Pneumonic phthisis, acute, 227 
Pneumothorax, 239 

amphoric breathing in, 221 

bulging of chest walls in, 195, 239 

cracked-pot sound in, 211, 212 

decrease of vocal fremitus in, 205 

in pleural effusion, 234 

physical signs of, 239 

tympanic note in, 211 
Pohl and Rosenbach's test, 236 
Poikilocytes, 385 
Poikilocytosis in chlorosis, 392 

in pernicious anemia, 392 
Poisoning, acute, alcohol, 50, 484 

anemia in chronic lead and arsenic, 
391 

anesthesia in toxic peripheral neu- 
ritis, caused by arsenic, lead, alco- 
hol, and mercury, 181 



Poisoning, appearance of tongue in acid 
or alkali, 117 

Argyll-Robertson pupil in bisulphide 
of carbon, 427 

arsenical, gait in, 60 

atrophy of tongue in chronic lead, 
120 

auto-intoxication, 470 

blue line on gums in lead, 60, 124 

brachial monoplegia in lead, 55 

cannabis indica, diagnosis of, 485 

chloral, symptoms of, 486 

chronic lead, paralysis in, 46 
gait in, 60 
silver, 136, 137 

constipation in phosphorus, 314 

contraction of pupil in opium, 485 

diplopia in ptomain, spigelia, co- 
nium, belladonna, gelsemium, 
413 

edema in arsenic, 163 

fatty casts in urine due to phos- 
phorus, arsenic, antimony, iodo- 
form, 347 

fever in septic, 459 

glycosuria in phloridzin, chloral, ar- 
senic, alcohol, and curare, 364 

greenish urine in salicylic acid, 339, 
340 

hemoglobinuria in mushroom, coal- 
tar, potassium chlorate, glycerin, 
338 

hyperesthesia in lead and arsenic, 
189 

inflammation of Steno's duct in sul- 
phuric acid, 126 

jaundice in phosphorus, 133 

in any poisoning causing exces- 
sive hemolysis, 134 

joint affections in chronic lead, 92 

mercurial tremors in, 48, 49 

myosis in chronic tobacco, 428 

neuralgia of head in lead and arsenic, 
537 

obstinate constipation in chronic 
lead, 415 

ocular paralysis in ptomain, alcohol, 
sulphuric acid, nicotine, lead, and 
carbonic acid, 421 

papillitis in alcohol and lead, 439 

paresthesia in aconite and carbolic 
acid, 187 

phosphorus, peptonuria in, 360 
stools in, 521 
vomit in, 523 

pin-point pupil in opium, 412 

pruritus in lead and opium, 190 

ptosis in gelsemium and conium, 24 

skin in malarial, 136 

slowness of breathing in opium, 
chloral, aconite, chloroform, anti 
mony, 201 



INDEX 



cm 



Poisoning, tremors of hand in chronic 
alcohol, lead, and mercurial, 49 
urine in .santonin and carbolic acid, 

339 
vomiting in antimonial, phosphorus, 

and arsenical, 517, 521 
wrist-drop in lead, 40, 50 
Poliomyelitis, acute, anterior, facial 
paralysis with monoplegia in, 20 
in infancy, hand in, 43 
ophthalmoplegia in, 419 
clawhand in, 43 
convulsions, headache, and muscular 

twitching in, 84 
crural monoplegia, 74 
diagnosis between acute central my- 
elitis and, 70 
paralysis of leg in, and acute 

cerebral paralysis, 87 
progressive muscular atrophy 
and, 75 

lexer in, SI, 87 

foot-drop in, 87 

gait in acute, 00 

lateral wrist-drop in, 40 

loss of knee-jerk in, 553 

of power in several muscles of 
limb later in disease in, 84, 88 

paraplegia in, 75, 84 

"Punchinello" leg in, 87 
Polychromatophilia, 385 
Polycythemia, chronic splenomegalic, 
393 

due to congenital cardiac disease in 
children, 382, 393 

in excessive diuresis, 393 

in tracheal stenosis, 393 
Polydipsia in diabetes niellitus, 303 
Polymorphonuclear leukocytes, 383 
Polyneuritis, differential diagnosis be- 
tween paraplegia in, and Landry's 

paralysis, 70 
Polynuclear leukocytes, 383 
Polyphagia in diabetes mellitus, 303 
Polyuria, 334 
Posthemiplegic chorea, 108 

epilepsy, 493 

tremor, 50 
Potassium ferrocyanide test for albu- 
min in urine, 357 
Pot-belly, 280 
Pott's disease, 72 

spastic paraplegia in, 72 
Pregnancy, caries of teeth in, 124 

chloasma of, 130 

discomfort due to, 5 

estimation of urea during, 309 

hemorrhagic retinitis in, 441 

pigmentation of eyelids during, 10 

prognosis of acute diffuse nephritis 
in, 372 

vomiting in. 520 



Presystolic mitral murmur, 249 
Prevost's symptom, 423 

Proctitis, symptoms of, 319, 320 
Progressive bulbar paralysis, bilateral 
facial paralysis in, 25 
muscular atrophy, spastic mono- 
plegia in, 74 
Prostate, enlarged, cause of interfer- 
ence with passage of urine. 333 
Prune-juice sputum in pneumonia, 227, 

529 
Prurigo, pigmentation of skin in, 137 
Pruritus about anus from opium, 190 
in chronic lead poisoning, 190 
in contracted kidnev, 190 
in diabetes, 190, 373 
in gout, 190 
in jaundice, 134, 190 
in piles, 190 
Pseudo-angina pectoris, pain in, 539, 

540 
Pseudobulbar paralysis, diagnosis of, 

25, 121, 559 
Pseudoleukemia, diagnosis of, 395 
Pseudomembranous dysentery, 320 
Pseudomeningitis, convulsions in chil- 
dren in, 503 
Pseudomuscular hvpertrophv, gait in, 

66 
Pseudoptosis caused by paralysis of 

the unstriped fibers of Midler, 23 
Pseudotabes, 60 

gait in, 60 
Pseudotetanus, Escherich's, •"><)} 
Psilosis, 118 
Psoriasis, nails in, 35 
Ptosis, alternate, in so-called nervous 
syphilis, 23 
associated with internal squint, 22 
caused bv affection of the sympa- 
thetic, 22 
by cerebral hemorrhage, 22 
by disease of the corpora quadri- 

gemina, 23 
by lesion of oculomotor nerve or 
nucleus, 22 
in angular gyrus, 22 
by nervous syphilis, 23 
by reflex irritation, 23 
complicating tetanus, 24 
concomitant symptoms of, if oculo- 
motor nerve is destroved, 22 
congenital, 22, 24 
in feeble, overworked women, 24 
in hysteria, 24 
in idiopathic muscular atrophv, 

24 
in locomotor ataxia, 24, 413 
in meningitis, 510 
in oculofacial paralysis, 20 
in recurrent paralysis of oculomotor 
nerve on one side, 25 



602 



INDEX 



Ptosis in tuberculous or syphilitic 
changes at base of brain, 24 
transient, in poisoning by gelsemium 

or conium, 24 
unilateral, 421 

with hemiplegia of face and limbs on 
opposite sides of the body, 25 
Puerile breathing, 220 
Puerperal eclampsia, diagnosis of con- 
vulsions in, 501 
melancholia, lingual spasm in, 123 
Puerperium, albumosuria in, 360 
Pulmonary abscess, 231 
sputum in, 530 
congestion, 232 
consolidation, position in, 5 
disease in children, pain in, 6 
edema, 232 
gangrene, 232 
breath in, 3 
position in, 5 
vomiting in, 523 
infarction, hemoptysis in, 529 
osteo-arthropathy, feet in, 88 
nails in, 35 

spade- like hands in, 40 
resonance, 210 
stenosis, 255 
Pulsating pleurisy, 207 
Pulsation, epigastric, 204, 305 

of retinal arteries in aortic regurgi- 
tation, 259 
on chest wall, 203 
Pulse, bloodvessels and, 265 
causes of rapid, 276 

of slow, 276 
Corrigan, 250, 259, 273 
dicrotic, 274 
examination of, 265 
feeble, rapid, and running, in rup- 
tured compensation of heart mus- 
cles, and in cholera morbus, 250, 
316 
force of, 267, 277 

hard and tense, in acute diffuse ne- 
phritis, 372 
high tension, in acute fevers, 277 

in chronic interstitial nephritis, 

372 
in C0 2 poisoning, 267 
in labor, 267 
in lead colic, 267 
in parenchymatous nephritis, 

277 
in renal colic, 267 
in acute alcohol poisoning, 484 

peritonitis, 273 
in aortic obstruction, 273 

regurgitation, 273 
in chloral poisoning, 486 
in opium poisoning, 485 
in uremic coma, 486 



Pulse, low tension in, exhausting dis- 
eases, 270 
in exophthalmic goitre, 269 
in mitral stenosis, 273 
in ruptured compensation, 273 
method of counting, 266 

of production of, 266 
of empty arteries in severe hemor- 
rhage, 275 
pulsus alterans, 274 

paradoxus, 274 
rapid and weak, in intestinal obstruc- 
tion, 513 
due to stimulation of heart, 277 
slow in cerebral tumor, 474, 509 

of digitalis, 273 
trip-hammer, 250, 259, 273 
water-hammer, 250, 259, 273 
wave, normal, 273 
Pulsus alterans, 274 

paradoxus, 274 
"Punchinello" leg, 87 
Pupil, Argyll-Robertson, 427 
in diabetes mellitus, 60 
in locomotor ataxia, 60 
contracted, 412 

from central nervous disease, 412 
from cerebral inflammation, 412 

tumor, 428 
from chronic tobacco poisoning, 

428 
from corneal inflammation, caus- 
ing photophobia, 412 
from locomotor ataxia, 428 
from meningitis, 412, 427 
from paretic dementia, 427 
in transverse myelitis, 78 
contraction and dilatation of, with 

Cheyne-Stokes breathing, 429 
dilated, 412 

from blindness, 412 

from fright, 412 

from glaucoma, 412, 428 

from hysteria, 412 

from intracranial pressure causing 

coma, 412 
from irritation of cervical sympa- 
thetic, 428 
of upper part of spinal cord, 
428 
from mydriatic, 412 
from paralysis of centre of third 

nerve, 428 
in acute croupous pneumonia, 428 

mania, 428 
in anemia of convalescence, 428 
in spinal meningitis, 428 
in tabes dorsalis, 428 
in tumors of spinal cord, 428" 
hippus, 429 

Hutchinson's, in cerebral hemor- 
rhage, 107 



INDEX 



603 



Pupil, immobile, 412, 427 

irregular and sluggish in syphilis, 

145, 441 
pin-point, in opium poisoning, 412 
reaction of, abnormal, 42(1 
to accommodation, 420 
to light, 420 
testing of, 420 
transitory, unequal dilatation of, in 

tuberculosis, 42!) 
Wernicke's sign of hemiopic inaction 
of, 428, 473 
Purpura hemorrhagica, 140 
hematemesis in, 518 
hematuria in, 338 
hemoptysis in severe, 529 
Henoch's disease in, 141 
in rheumatism, 140 
joint involvement with fever in, 
400 
Pus casts in urine, 346 
in stools, 324 
in urine, 342 
Pustular syphilodeim, 153 
Putrid bronchitis, 240 
Pyelitis caused bv .Strongylus gigas, 
338 
chills and fever in, 342, 459 
diagnosis of, 342 
fever in, 342, 459 
pain in, 342 
pvuria constant or intermittent in, 

342 
urine acid in, 342 
Pvelonephrosis, casts of micrococci in, 

"346 
Pyemia, chill in, 442 

diazo-reaction in severe, 370 
'jaundice in, 135, 136 
joint involvement with fever in, 466 
parotitis in, 33 
profuse sweating in, 161 
Pyemic abscess of liver, 303 
Pylephlebitis, vomiting in, 522 
Pvopneumothorax, coin percussion in, 
235 
Hippocratic succussion in, 226 
metallic tinkling in, 222 
subphrenicus, 305 



Quincke's sis;n in aortic regurgitation 
259 



Railroad-bridge tremor, 50 
Rales, 222 

altered bv couching if not crepitant, 
222j 



Rales, bubbling, 222 

character of, in asthma, 241 
crepitant, 222 
dry, 222 
moist, 222 

redux, in pneumonia, 227 
sonorous, 222 
Raynaud's disease, coma in. 1^» 
gangrene in. 39, 15s 
hands in, 35 
hemoglobinuria in, 340 
localized sweating in, 161 
skin in, 138 
svmptoms of, 158 
Rectal catarrh, acute, 319, 320 
Reflex iridoplegia. See Argyll-Robert- 
son pupil, 
paralysis, 84 
Reflexes, ankle clonu-. 55.") 
biceps tendon, 58, 552 
chin-jerk, 552 
cremasteric, 552 
diseases in which decreased, 553 

in which increased, .')^)\ 
in transverse myelitis, 77 
knee-jerk, 552 

loss of ocular, in acute alcoholic poi- 
soning, 484 
of skin. 554. 555 
plantar. 555 
scapulohumeral of von Bechterew, 

552 
tendon, 552 
Regurgitation, aortic, 250 
pulse in, 273 
mitral, 247 

pulse in, 273 
tricuspid, 255 
Relapsing fever, edema of legs and 
wrists in. 165 
fever in, 452 
hematemesis in, 518 
hyperesthesia in, 189 
jaundice in, 134 
spirillum of Obermeier in blood 

in, 453 
sweating in. 161 
tongue in, 114 
Remittent fever. See Malaria, remit- 
tent. 
Renal colic, retraction of abdominal 
wall in, 281 
disease, albumin in urine in, 359 
anemia in, 391 
diarrhea in, 317 

pumness under eyes in, 10, 14. 411 
Resonance, vocal, 222, 224 
Baccelli's sign. 225 
decreased, causes of, 225 
increased, causes of, 225 
Respiration, causes of labored, 201 
of rapid, 200 



604 



INDEX 



Respiration, causes of slow, 201 
Cheyne-Stokes, 201 
costal, 202 
counting, 200 
diaphragmatic, 202 
in children, 8 
in chloral poisoning, 486 
in coma of apoplexy, 488 
in diabetic coma, 487 
in healthy child, 8 
in uremic coma, 487 
inspiration prolonged in spasmodic 

croup, 201 
prolonged expiration in asthma and 

emphysema, 200 
ratio of pulse to, 200 
rhythm of, 201 
stertorous, 484 
wavy, in pneumonia, 203 
Retention cysts of pancreas, 304 
of urine in locomotor ataxia, 331 
in myelitis, 330 
in overdistention, 332 
in pressure during childbirth, 331 
Retina, edema of, in arterial disease, 

441 
Retinitis, 440 
albuminuric, 440 
hemorrhagic, 440 
in diabetes, 441 
in leukemia, 395 
in syphilis, 440 
Retrobulbar neuritis, 439 
Retro-esophageal abscess, 124 
Rheumatic form of gonorrheal arthri- 
tis, 89 
Rheumatism, acute articular, chlorides 
decreased in, 370 
increased in, in convalescence, 
370 
convulsions in, 466 
cyanosis in, 466 
erythema in, 140 
fever in, 465 
hands in, 38 
headache in, 471 
in knee or ankle, 90 
iritis in, 441 
joint affections in, 466 
papillitis in, 439 
purpura in, 140 
spontaneous dislocation of the 

hip following, 92 
subcutaneous fibrous nodules 

in, 142 
sweating of, 161 
tongue in, 114 
uric acid in urine of, 351 
urticaria in, 143 

with hvperpyrexia, delirium in, 
466 
chronic, hand in, 38 



Rheumatism, chronic, limping gait in, 
59 

gonorrheal, 89 

of scalp, symptoms of, 538 
Rheumatoid arthritis. See Arthritis 

deformans. 
Rhonchi, 222 
Ribs, systolic retraction of, in adherent 

pericardium, 204 
Rickets, beaded ribs of, 198, 199 

carpopedal spasm in, 46 

craniotabes in, 31 

deficient bony development in, 31 

early decay of teeth in, 124 

excessive sweating of head in, 33 

gait in, 66, 69 

Harrison's grooves in, 198 

head in, 12, 31 

hyperesthesia in, 189 

laryngeal spasm in, 242 

nodding spasm in, 28 

open fontanelle in, 31 

pain in back in, 541 

pigeon breast in, 198 

pseudoparaplegia in, 85 

spastic paraplegia in, 71 

subperiosteal hematoma in, 91 

sweating of head in, 161 

tenderness of skin in, 189 
Rigidity, intestinal, 309 
Risus sardonicus in epilepsy, 491 

in tetanus or strychnine poisoning, 
10, 28 
Roberts' yeast test for sugar in urine, 

363 
Romberg's symptoms, 60, 83 
Rontgen rays in diagnosis of stricture 
of esophagus, 126 
of tuberculosis, 231 
Rose rash, 144. See Erythema and 

Roseola. 
Rotheln, appearance of rash in, 145 

fever in, 454 

symptoms of, 145 
Rubella, 145. See Rotheln. 
Rubeola, 145. 
Rupia, 159 



Saccharomtces albicans, causing fer- 
mentation in diabetic urine, 355 

St. Vitus' dance. See Chorea. 

Salaam convulsions, 506 

Salivary calculus, 126 

Saltatoric spasm, 507 

Sand, intestinal, 324 

Saprophytic organisms a cause of em- 
pyema, 239 

Sarcime ventriculi in vomitus from 
chronic gastric catarrh, 519 



INDEX 



605 



Sarcinae ventriculi, in vomitus from 
gastric cancer, 520 

from dilatation, 520 

from ulcer, 520 
test for, 520 
Sarcoma, anemia due to, 391 
enlargement of Liver in, 301 
purpura in multiple, 142 
Scalp, rheumatism of, pain in, 538 
"Scaphoid" belly, 281 
Scapulohumeral reflex of von Bech- 
terew, 552 
in neurasthenia, 552 
Scarlet fever, arthritis in, 92 

Cheyne-Stokes respiration in, 201 

chill in, 442 

collar of brawn in, 453 

date of eruption in, 147 

diazo-reaction in severe, 370 

enlargement of spleen in, 310 

erythema in, 1 15 

fever in, 453 

gangrene of lower extremities 

alter, 95 
glvcosuria during convalescence, 

364 
hematuria in, 335 
lysis in fever of, 453 
otitis in, 453 

pleurisy with effusion complicat- 
ing, '238 
prognosis from lexer, 453 
rose rash in, 145 
sore throat in, 128 
splenic enlargement in, 310 
spontaneous dislocation of hip fol- 
lowing, 93 
strawberry tongue in, 115 
synovitis in, 39 
Schonlein's disease, joint involvement 
in, 92 
symptoms of, 141 
ulcer of buccal mucous membrane 

in, 126 
ulcerations of tongue in, 118 
Sciatica. See Neuritis, sciatic. 
Sciopedy, 88 
Sclerema neonatorum, symptoms of, 

144 
Sclerodactyle. nails in, 35 
Scleroderma of tongue, 120 

skin in, 17, 143 
Sclerosis, amyotrophic lateral. 44 
alterations of hands in, 44 
ankle clonus in, 555 
Argyll-Robertson pupil in, 427 
character of speech in, 559 
knee-jerk increased in. 554 
spastic paraplegia in, 71 
disseminated, 187 
ankle clonus in, 555 
coma in, 490 



Sclerosis, disseminated, convulsions in, 

503 
differential diagnosis of, 64, 427 
expression of face in. 1 1 

gait in. (it 

hemianesthesia in, 170 
hemiplegia resulting from, 109 
hippus in, 429 
knee-jerk increased in, 554 
nystagmus in, 425 
optic atrophy in. 440 
paralvsis of ocular muscles in. 
419 

of tongue in, 122 
slow, scanning speech in. 04. ~)~> ( .) 
spasm of tongue in, 123 
symptoms of. 51 
tremor of hands in. l!i 

of head in. 50 
vertigo in. is;; 
general arterial accentuation of 

heart sounds in. 245 
lateral, absence of vesical svmptoms 
in, 331 
ankle clonus in. ^~)~) 
gait in, (>0 

increased reflexes in. 71 
primary, knee-jerk in. 551 
spastic paraplegia in. 71 
multiple cerebrospinal, 71 
Scorbutus. See Scurvy. 
Scotoma 439 

Scrofulosis, abdomen in, 281 
dactylitis in, 35 
tongue in, 115 
Scurvy, corneal ulceration in. 441 
dropsy in, 164 

ecchymosis under the eyes in. 10 
hematemesis in. 518 
hematuria in, 338 
loosening of teeth in, 124 
pain in back in, 541 
petechia 1 in, 142 

pseudoparalysis in, in infancy, 85 
skin in, 189 

sponginess of gums in. 124 
Seal-fin hands in arthritic deformans 

and gout. 37 
Senile chorea. 47 

gangrene of foot. 95 
Senility, tremor of hands in, 49 
Septicemia, blood in. 265 

Cheyne-Stokes respiration in. 201 

diarrhea in. 321 

fever in. 459, 463 

great variations in temperature in, 

463 
jaundice in, 133 
petechia? in, 142 
retinal hemorrhages in. 441 
rose rash in, 148, 149 
splenic enlargement in, 311 



606 



INDEX 



Shiga's bacillus, epidemic dysentery- 
due to, 320 
Sibilant rales, 222 
Singultus, 508 

causes of, 508 
Skin, anesthesia of, 168 
cadaveric, in pyemia, 136 
cold and moist, with high rectal 
temperature, in sunstroke, 466 

and wet, a bad symptom in fever, 
445 
color of, in health and disease, 129 
cyanosis of, 138, 139 

due to laryngeal obstruction, 139 

from drugs, 139 

in cardiac disease, 139 

in newborn, 139 

in paretic dementia, 139 
dropsy and swelling of, 143, 162 
dry and hot, in fever, 445 
edema of, 143 

eruptions of, in disease, 139 
excess of dryness of, 161 
gangrene of, 158 
glossiness of, 157 
greasy yellow, in phthisis and chronic 

liver disease, 136 
greenish yellow, in chlorosis, 136 
harsh and dry, in acute diffuse ne- 
phritis, 372 
in cholera, 161 
in diabetes, 161, 162, 373 
hemorrhages into, 142 
hyperesthesia of, 188 
in acute alcohol poisoning, 484 
in Addison's disease, 137 
in angioneurotic edema, 143 
in argyria, 136, 137 
in carcinoma of internal organs, 136, 

138 
in chloasma of pregnancy, 136 
in chromophytosis, 137 
in edema neonatorum, 144 
in elephantiasis, 143 
in influenza, 189 
in jaundice, 129, 130 
in kidney disease, 138 
in myxedema, 143 
in ochronosis, 136 
in opium poisoning, 189 
in profound anemia, 189 
in sclerema neonatorum, 144 
in scleroderma, 143 
in tuberculosis, 136 
increased sensibility of, due to ergot, 

189 
leukoderma, in true goitre, 138 
muddy yellow, in chronic malaria 

and prolonged suppuration, 136 
pain of, 190 
pallor of, 138 

in chlorosis, 138 



Skin, pallor of, in myxedema, 138 

in nephritis, 138 

in Raynaad's disease, 138 

in vitiligo, 138 
parchment-like, in syphilis, 10 
pigmentation of, 136 

by the prolonged use of arsenic, 
137 

due to scratching, 137 
paresthesia of, 186 
pigmentation of, due to pediculi, 137 

in exophthalmic goitre, 137 

in prurigo, 137 
pruritus of, 190 
redness of, 142 
scars of, 160 
sensation of, 165 
sweating of, 160 
table of reflexes of, 556 
tache cerebrale, 144 

meningeale, 144 
tactile sensibility of, 165 
tenderness of, in diseases of internal 
organs, 189 

in rickets, 189 
thermal sensibility of, 165, 166 
waxy, in cretinism, 15 
yellow, in xanthoma, 136 

and greasy, in paretic dementia, 
136 
Skodaic resonance, 212 
Sleeping sickness, 405 
Smallpox, appearance of, eruption in, 

146, 152, 454 
date of eruption in, 147, 152 
fever in, 454 
grisolle sign of, 147 
headache in early stage of, 481 
hemoptysis in hemorrhagic, 529 
pain in back in onset of, 454, 551 
peptonuria in, 360 
Smokers' patch on tongue, 119 
Snake-bite, purpuric eruptions follow- 
ing, 141 
Sonorous rales, 222 
Spasm, blepharofacial, 27 
facial, Abadie's sign in, 27 

in blepharofacial spasm, 27 

in chorea, 271 

in convulsive tic, 272 

in epilepsy, 273 

in hysteria, 285 

in meningitis, 27, 286 

in tetanus, 27, 287 
habit, 26, 474 

hysterical, of esophagus, 125 
laryngeal, 242 

nodding, 28. See Nodding spasm. 
Spasms, 504 
carpopedal, 46 
in adults, due to locomotor ataxia, 

242 



INDEX 



mi 



Spasms in adults, due to mediastinal 

growths, 242 
in children, due to croup, 242 

due to digestive disturbances, 242 

due to laryngeal catarrh, 242 
. due to rickets, 242 
in chorea insaniens, 505 

minor, 505 
in electric chorea, 506 
in Huntingdon's chorea, 500 
in lesion of middle peduncle of cere- 
bellum, 507 
in paramyoclonus multiplex, 506 
in Thomsen's disease, 507 
in true chorea, 505 
laryngeal, in adults, 242, 243 
of fingers due to occupation, 46 
of tongue, 123 
saltatoric, 507 
varieties of, 504 
Spastic infantile hemiplegia, 44 
monoplegia, 74 
paralysis, hereditary, 73 
paraplegia, cerebral, 69 

spinal, 72 
rigidity of arms, 10 
Specific gravity, method of estimating 
hemoglobin, 388 

of urine, 342 
Speech, 557. See also Voice, 
defects of, 559 

agraphia, 560 

alexia, 560 

aphasia, 559 
conduction, 560 

aphemia, 560 

apraxia, 560 

paraphasia, 560 

tests for, 561 

word blindness, 560 
deafness, 560 
feeble, hesitating, in pneumonia of 



pulmonary edema, 558 
ilting, hesit 



halting, hesitating, in paretic de- 
mentia, 559 
incoherent, in chorea in children, 559 

in delirium, 559 
indistinct, mumbling, 558, 559 
nasal, in adenoid vegetation, 558 
nervous, mechanism of, 560 
scanning, in multiple sclerosis, 64 
shrill, piping, 559 

slow, scanning, in disseminated 
sclerosis, 559 
in Friedreich's ataxia, 559 
tests for defects of, 561 
whispering, causes of, 557 
Spermatorrhea. 354 

accompanying oxaluria, 351 
Spermatozoa in urine, significance of, 

354 
Sphygmocardiograph, Jacquet's, 276 



Sphygmograph, 274 

Sphygmomanometer, 270 
Spinal cord, rise in temperature due to 
injuries of, 467 
hemorrhage into, 75 
knee-jerk in injuries of, 55:1 55 1 
localization of functions of seg- 
ments of, 7!», 82 
location of lesion of, in anesthesia, 

80, 175 
tumor of, paraplegia in, 84 
irritation, dilatation of pupil in, 428 
Spine, caries of, symptoms of, 541 
Spirillum of Obermeier in blood in re- 
lapsing fever, 453 
Spleen, causes of enlargement of, 310 
of extension downward, of, 31 1 
enlarged, in amyloid disease of kid- 
ney, 310 
in Banti's disease, 31 1 
in hepatic cirrhosis, 310 
in leukemia, 310, 395 
in malarial fever, 310 
in scarlet fever, 310 
in syphilis, 310 
in typhoid lever, 310 
floating, 312 
swelling of, in septicemia, 311 

in Weil's disease, 160 
uric acid in enlargement of, 351 
Splenic anemia, 310 

lexer. Sir Anthrax. 
Spontaneous dislocation of the hip 

after infectious diseases, 92 
Spots of Yalleix, 539 
Spotted fever. See Cerebrospinal men- 
ingitis, 
Sputum, actinomyces in, 533 
anchovy sauce, 530. 
blood-streaked, 529 
bloody, 529 

brick-dust, in hepatic abscess, 520 
brownish, in gangrene of Lungs, 232 
casts of bronchioles in, 531 
Charcot-Levden crvstals in asth- 
matic, 241, 531 
copious and purulent, 232 
crystals of margaric acid in pulmo- 
nary gangrene, purulent bron- 
chitis, and follicular tonsillitis, 532 
Curschmann's spirals in, 241, 531 
Dittrich's plugs in, 240 
eggs of Distoma pulmonum in. 533 
elastic fibers in, 532 
frothy, 232. 530 
hooks of echinococcus in, 533 
in asthmatic attacks, 530 
in chronic bronchitis. 240 
in pulmonary gangrene. 232, 530 
liquid and watery, 530 
prune-juice, 226/529 
purulent, causes of, 530 



608 



INDEX 



Sputum, rusty and sticky, 528, 529 
semiliquid, 530 

staining for tubercle bacilli in, 534 
thick and yellowish, 528 
Squint, diagnosis between concomitant 
and paralytic, 414 
of conditions producing, 418 
external and internal, due to tumor 
at base of brain, 473 
causes of, 419, 420, 421 
in hysteria, 425 
in meningitis, 510 
in ocular palsy, 22, 416 
internal, causes of, 420 
significance of external, 421 
Staphylococci a cause of empyema, 

239 
Status epilepticus, 498 
Stellwag's symptom, 412 
Stenosis, aortic, 250 
pulse in, 273 
mitral, 249 

pulse in, 273 
pulmonary, 255 
tracheal, polycythemia in, 393 
Steppage gait, 60 
Stereognosis, 166 
Stokes- Adams disease, 263 

epileptiform seizures in, 502 
Stokvis modification of Jaffe's test for 

indican, 365 
Stomach, cancer of, 290 

cough due to reflex irritation from, 

525 
dilatation of, 295 

vomiting in, 519 
distention of, by gas, 296 
examining of, with gastrodiaphane, 

296 
hour-glass, 299 
indicanuria in cancer of, 341 
palpation and percussion of, 287 
test of contents for hydrochloric 
acid, 299 
for lactic acid, 299 
for urates in urine in disorders of, 
350 
ulcer of, 291 

vomiting in dilatation of, 519 
Stomatitis, action of child with, toward 
breast, 7 
buccal mucous membrane in, 126 
impetiginosa, 120 
malignant ulcerative, 126 
offensive odor of breath in, 3 
temperature of mouth raised in, 

444 
tongue in ulcerative, 118 
Stone in bladder, 332 
Stools. See also Feces, 
bilious, 322 
bloody, 322, 515 



Stools, clay-colored, in hepatogenous 
jaundice, 134 
in Weil's disease, 460 
gallstones in, 324 
in cholera, comma bacilli in, 317 

infantum, 316 
in dysentery, 319 
in intussusception in children, 512 
in proctitis, 319 
intestinal parasites in, 324 
mixed with mucus, 322 
oily, in carcinoma of pancreas, 294 
pus in, 324 

ribbon-shaped, in follicular entero- 
colitis, 318 
rice-water, in antimonial poisoning, 

317 
tarry, in yellow fever, 460 
Strabismus. See Squint. 
Strawberry tongue, 115 
Streptococci a cause of empyema, 239 
Stricture of esophagus, 125. See Eso- 
phageal stricture. 
Strongylus gigas, hematuria due to, 338 
Stupor in typhoid fever, 449, 451 
in ulcerative endocarditis, 451 
Subdural hemorrhage, 489 
Subnormal temperature, 467 
Subperiosteal hematoma, 91 
Subsultus tendinum, 36, 51 
Succussion, Hippocratic, 226 

in pleural effusions with pneumo- 
thorax, 235 
Sudamina, 161 
Sugar in the blood, 408 

Williamson's test for, 408 
in urine. See Glycosuria and Urine. 
Summer complaint, 316 
Sunstroke, character of fever in, 466 
diagnosis of coma in, 490 
headache of, 481 
skin cold and moist in, 466 
hot and dry in, 466 
Suppurative processes, peptonuria in, 
360 
tonsillitis, symptoms of, 126 
"Surgical scarlet fever," 149 
Sweat, bile-stained, in jaundice, 161 
Symmetrical gangrene, 158 
Syncope, diagnosis of, 502 
Synovitis, acute, 90 
Syphilis, action of child with, toward 
breast, 7 
alternate ptosis in, 23 
aortitis in, 540 
Argyll-Robertson pupil in cerebral, 

427 
at base of brain, 25 
broadness of bridge of nose in con- 
genital, 12 
cerebral, coma in, 490 
hemiplegia in, 109 



IXDEX 



609 



Syphilis, cerebrospinal, multiple, 64, 65 
cutting of teeth in inherited, 124 
diagnosis between cerebrospinal 
syphilis and disseminated scle- 
rosis, 427 

of coma in, 490 

of ep lepsy due to, 494 
enlargement of spleen in early, 310 

of tongue in, 118 
eruptions of, 148, 149, 159 
fever in, intermittent, 465 

remittent, 465 

simple, continued, 465 
fingers in dactylitis in, 35 
fissures and chancres of tongue in, 

118 
gummatous swelling and periosteal 

thickening of shins in. 93 
Hutchinson teeth in, 124 
immobility of pupil in, 427 
iritis in, 441 
irregular pupil in. 145 
miscarriage a symptom of. 5 
mucous patches about mouth and 

anus in infantile, 12 
nails in, 35 
of intestinal tract, diarrhea due to, 

321 
open fontanelle in. 31 
pain in periostitis of skull in, 538 
papillitis in, 439 
parchment-like skin of. 10 
paresthesia in spinal, 186 
pseudopalsy in. 55 
ptosis in changes at base of brain in, 

22 
purpura in, 141 

purulent acne of forehead in, 153 
retinitis in, 441 
rose rash in, 148, 149 
scars in, 160 

spastic paraplegia in spinal, 72 
symptoms of arteritis due to. 474 
ulceration of tongue in. 117 
Syphilitic arteritis. 474 

paralyses in, 20 
epilepsy, 494 
gumma, 474 
meningitis, 474 

periostitis of skull, pain in, 538 
rupia. 159 
triad, 124 
Syphiloderm, pustular, 153 
Syringomyelia, nails in. 35 

necrosis of terminal phalanges in, 39 

pain and temperature sense in. 175 

partial anesthesia in, 175 

patches of anesthesia in. 175 

small joints affected in, 89 

symptoms of. 175 

wasting of hands with anesthesia in, 

44 

39 



Tabes dorsalis. See Locomotor ataxia. 
Tabetic atrophy of foot, 89 
of optic nerve, 440 
ulcer, 95 
Table of reflex*-. 556 
Tache cerebrale, 1 1 1 

meningeale, 1 1 1 
Tachycardia. 203. 277 
Tactile sensibility of skin. 165 
Talipes equinovarus in Friedreich's 

ataxia, 63 
Tallquist's method of estimating hemo- 
globin. 399 
Tape-worm. See Parasites; Tenia. 
Taste, decrease of aci lity in. of facial 
hemiatrophy, 16 
loss of, in anterior portion of tongue 
in disease of petrous portion of 
temporal hone. 18 
Tenia cucumerina. 327 
mediocanellat a. 326 
solium, 326 
Teeth, ages at which different, appear 
in children. 124 
blue line around, in lead poisoning, 

124 
caries of, in diabetes mellitus, 121 

in pregnancy, 124 
decay of, in rickets. 124 

early, in inherited syphilis, 121 
grinding of. in children, 124 
Hutchinson. 124 
loosening of, in salivation. 124 

in scurvy. 124 
staining of, 124 
Teichmann's crystals in hemoglobin- 
uria, 340 
Temperature. See also Fever, 
in acute alcohol poisoning. 4^4 
in cholera Asiatica. 316 

infantum. 316 
in diabetic coma. 486 
in injuries to cervical cord, 467 
in intestinal obstruction, 513 
in typhoid fever, 447 
in uremic coma, 486 
subfebrile, mildly febrile, decidedly 

febrile. 442 
subnormal, causes of, 467 
in cretinism. 15 
in heart exhaustion. 467 
in injuries to dorsal portion of spi- 
nal cord. 467 
in pernicious malaria, 467 
Tendon reflexes. 552 
Tenesmus in bladder trouble. 329 
in cholera infantum. 316 
in dysentery. 319 
in intussusception. 512 
in proctitis. 319. 320^ 



010 



INDEX 



Tenesmus in stricture of rectum, 318 
Tension, arterial, 267 

asynchronous, of sigmoid valves caus- 
ing reduplication of second sound 
of heart, 246 
Terminal leukocytosis, 396 
Tetanus, convulsions in, 503 
facial spasm in, 27, 28 
head or cephalic, 29 
knee-jerk increased in, 554 
ptosis in, 24 

risus sardonicus in, 10, 28 
Tetany, "accoucheur's hand." in, 46, 
504 
character of convulsions in, 504 
Chvostek's symptom of, 504 
Erb's symptom of, 504 
gastric dilatation in, 46 
laryngismus stridulus in, 504 
thyroid, wasting in, 46 
Trousseau's symptom of, 504 
Thermic fever. See Sunstroke. 

sensibility of skin, 166 
Thoma-Zeiss' hematocytometer, 376 
Thomsen's disease, diagnosis of, 507 
spasm of hand, in, 48 
of tongue in, 123 
Thorax, anemysm of, diagnosis be- 
tween medicinal growths and, 
243 
localized sweating in, 161 
spongy, venous masses above 
clavicle due to, 202 
inspection of, 191 
Thread-worms, 327 
Thrill, causes of, 207 

diffuse and feeble, in cardiac dilata- 
tion, 260 
in aortic aneurysm, 251 
in carotid arteries, 263 
in hydatid, cyst of liver, 304 
in mitral regurgitation in children, 
248 
stenosis, 249 
Thrombosis, cerebral, 45 

brachial monoplegia in, 52 
bulging fontanelle in, 108 
coma in, 489 
edema in, 162, 164 
hemiplegia in, 108 
of lateral sinus, Gerhardt's symp- 
tom of, 480 
of superior longitudinal sinus, 479 
of cavernous sinus, 480 
of coronary artery, 264 
of femoral artery, 93 
of lateral sinus, 480 

localized edema in, 164 
of umbilical vein in melena neona- 
torum, 518 
of vena azygos a cause of serous 
pleural effusion, 236 



Thrombosis, vomiting in, 509 
Thrush, tongue in, 115 
Thyroid wasting in tetany, 46 
Tic, convulsive, 48 

facial spasm in, 26 
Tinnitus aurium in Meniere's disease, 

522 
Tobacco amblyopia, 440 

heart, 263 
Toe, tender, in sciatica, 542 
Toes, separation of, in ainhum, 95 
Toison's solution for counting white 

corpuscles, 379 
Tongue, annulus migrans of, 120 

bilateral atrophy of, 120 

biting of, 119 

chancre of, 118 

chronic superficial glossitis of, 119 

coating of, unilateral, due to decayed 
teeth or hemiplegia, 116 

dryness or moisture of, 116 

enlargement of, in acromegaly, 121 

epithelioma of, 118 

eruptions of, 119 

examination of, 112 

in children best when crying, 8 

fibrillary tremor of, 123 

fissures of, 117 

geographical, 120 

glossodynia exfoliativa of, 119 

hemiatrophy of, 121 

ichthyosis of, 119 

in acute articular rheumatism, 114 
catarrhal jaundice, 114 
gastric catarrh, 115 
in children, 115 
inflammation of, 120 

in Addison's disease, 117 

in advanced disease of exhausting 
nature, 116 

in anemia, 116 

in biliousness, 114 

in cardiac disease, 116 

in cretinism, 15 

in dysentery, 116 

in grave disease of the viscera, 116 

in hemiplegia, 116 

in hepatic abscess, 116 

in mucous disease, worm-eaten, 115 

in persons taking large amounts of 
milk, 115 

in poisoning by acids, 117 
by alkalies, 117 
by cantharides, 117 
by corrosive sublimate, 117 

in pulmonary disease, 116 

in relapsing fever, 114 

in scarlet fever, 115 

in scrofulosis, 115 

in stomatitis impetiginosa, 120 

in syphilis, 117 

in thrush, 115 



INDEX 



611 



Tongue in tonsillitis, 113 
in typhoid fever, 113 
in ulcerative stomatitis, 118 
in uremia, 114 
leukokeratosis of, 119 
leukoma of, 119 
lichen planus of, 120 
movements of, 121 
mucous patches of, 118 
mycosis of, 115 
edema of, 120 
paralysis of, 121 
parrot, 116 
patches on, 119 
purple spots on, in Addison's disease 

117 
scleroderma of, 120 
smokers' patch on, 119 
spasm of, 123 
stains of, 116 

strawberry, in scarlet fever, 115 
tremor of, in alcoholism, 123 

in glossolabiopharvngeal paralysis, 
123 
ulceration of, 118 
unilateral atrophy of, in chronic lead 

poisoning, 120 
urticaria of, 119 
wandering rash of, 120 
worm-eaten, in mucous disease, 115 
xanthelasma of, 117 
xeroderma pigmentosum of, 119 
Tonsillitis, breath in, 3 

chronic night cough in, 527 
crvstals of margaric acid in follicu- 
lar, 532, 533 
diagnosis between diphtheria, scarlet 

fever, and, 127 
dysphagia in, 124, 125, 127 
fever in, 126 
odor of breath in, 3 
symptoms of, 126 
tongue in, 113 
Tonsils, chronic cough in enlarged lin- 
gual, 527 
night cough in enlarged faucial, 527 
pain in calculus of, 128 
symptoms of chronic enlargement of, 
128 
Torula cerevisise causing fermentation 

in gastric dilatation, 519 
Tracheal tugging in aneurysm, 254 
Transitional leukocytes, 383 
Transudations into pleural cavities, 236 
Traube's semilunar space obliterated in 

left-sided pleural effusion, 234 
Tremor of hands and arms, 49 

in disseminated sclerosis. 49 

in general paresis, 50 

in Graves' disease, 50 

in hysteria, 50 

in mercurial poisoning, 48, 49 



Tremor of hands and arm.- in paraly- 
sis agitans, 49 
railroad-bridge type of, 50 

of tongue. 122 

of type Rendu, 51 

posthemiplegic. 50 

sometimes found instead of occupa- 
tion spasm, 46 
Trichiniasis, diagnosis of, 452 

leukocytosis in, 396 

puff\ r eyelids in, 14 
Trichinosis. See Trichinia 
Trichloracetic acid test for albumin in 

urine. 357 
Trichocephalus dispar, 328 
Tricuspid regurgitation, 255 

stenosis, 255 
Trimanual percussion, 309 
Trip-hammer pulse of aortic regurgita- 
tion, 250, 259, 273 
Trommer's test for sugar in urine. 363 
Tropical abscess of liver, 303 

dysentery, 319 
Trousseau's symptom of tetany. 504 
Trypanosoma in blood. 405 
Tube casts. See Casts. 
Tubercle bacilli, examining and stain- 
ing of, 534-536 

in urine, 353 

of chancroid. 177 
\ Tuberculosis a cause of empyema. 23s 

amphoric breathing in, 221, 230 

anemia in, 391 

bronchial breathing and consolida- 
tion in, 219, 220 

bronchitis a cause of death in. i» 

bronchophony in, 230 

bubbling rales in. 222, 229 

( narcot-Leydcn crvstals in. 531 

Cheyne-Stokes breathing in menin- 
geal, 201 

chill in, 442 

chronic loose morning cough in. 526 

cracked-pot sound in, 211, 212 

crepitant rales and breaking down of 
lung tissue in, 222 

cyanosis in acute miliary. 464 

dactylitis in. 35 

diagnosis between catarrhal pneu- 
monia and pulmonary, 229 

diarrhea of, 319 

diazo-reaction in severe pulmonary, 
370 

elastic fibers in sputum of. 532 

expiration prolonged in, 229 

fever in acute miliary, 464 
pulmonarv. 463 

frog-belly in, 281 

heavy face in bone disease in. 12 

hectic fever in, 230 

hemoptysis in, 529 

hemorrhagic pleurisy in. 23^ 



612 



INDEX 



Tuberculosis, hoarseness in, 557 
hollow-chested build in, 1 
leukocytosis in, 451 
loss of flesh in, 230 
mammary glands enlarged in, 199 
metallic tinkling in, 222 
multiple ulceration of tongue in, 118 
necessity of examining axilla in, 232 
ocular palsy in, 419 
of bladder, hematuria due to, 338 
of kidney, 337, 548 
of mesenteric glands, 294 
of omentum, 294 
pectoriloquy in, 230 
peptonuria in, 360 
percussion note dull in consolidation 

due to, 211 
pleurisy complicating, 236 
ptosis in changes at base of brain due 

to, 24 
puerile breathing an early sign of, 

220 
rapidity of breathing in, 200 
retraction of abdominal wall in, 281 
Rontgen rays in diagnosis of, 231 
scars on neck from suppurating 

glands in, 160 
spirituelle face of children with di- 
athesis of, 12 
sputum, Curschmann's spirals in, 

530 
sweating in, 161 
tongue in, 116 
transitory, unequal dilatation of 

pupils in, 429 
vocal fremitus and resonance in- 
creased in, 205, 225, 229 
vomiting in acute miliary, 510 
Wintrich's change of percussion note 

in, 230 
Tuberculous glands, symptoms of, 294 
meningitis, 476 

differential diagnosis of, 476 

headache in, 476, 477 

in children, 477 

Kernig's sign in, 479 

lumbar puncture in, 478 

papillitis in, 439 
pyelitis, 342 
Tubular breathing, 219, 220 
Tumor, abdominal, pain in, 548 
at base of brain, symptoms of, 20 
bone, Bence-Jones albumin in, 355 
brain, Cheyne-Stokes breathing in, 
201 

contracted pupil in, 428 

hyperesthesia in, 189 

impaired memory in, 509 

monoplegia in, 53 

papillitis in, 439, 510 

paresthesia in, 186 

severe headache in, 509 



Tumor, brain, slow pulse in, 509 
spastic hemiplegia in, 109 
symptoms of, 473 
unilateral anesthesia in, 171 
vertigo in, 483, 509 
vomiting independent of taking 
food in, 509 
diagnosis of fatty, in abdominal wall, 

289 
in intussusception, 512 
in renal pelvis, symptoms of, 547 
of abdomen, 289, 294 
of bladder, 332 

of cord, bladder symptoms of, 332 
dilatation of pupil in, 428 
girdle sensation in, 188 
of lung, rapid respiration in, 200 
of mediastinum, 242 
of nerves, pain in, 551 
of omentum, 294 
paraplegia in, 84 
phantom, 309 
pontine, anesthesia in, 172 
Tympanites in flatulent colic, 280, 
281 
in intestinal obstruction, 514 
in peritonitis, 281 
in typhoid fever, 281, 451 
Typhoid fever, bacillus of Eberth the 
cause of, 451 
bed-sores in, 158 
blood in, 395 
bloody stools in, 322, 515 
■ bradycardia in, 263 
carphologia in, 51 
Cheyne-Stokes respiration in, 201 
chill in, 442 
coma in, 486, 487 
delirium in, 13, 451 
diagnosis, 451 

between acute miliary tubercu- 
losis and, 451 
Malta fever and, 452 
relapsing fever and, 452 
remittent fever and, 449 
trichiniasis and, 452 
typhus fever and, 452 
ulcerative endocarditis and, 
451 
edema of thigh over deep muscular 

abscess following, 164 
Ehrlich's diazo-reaction in, 370 
enlargement of spleen in, 310, 451 
eruption in, 149, 449 
face in, 13 
fever in, 446 

gangrene of lower extremities fol- 
lowing, 95 
glycosuria in convalescence in, 364 
headache in, 482 

hyperesthesia in convalescence 
from, 189 



INDEX 



613 



Typhoid fever, hypertrophic osteoar- 
thritis following, 91 

in children, 459 

increase of urine in convalescence 
from, 334 

lesions of lungs in, 451 

leukocytosis absent unless perfo- 
ration occurs during, 396, 452 

meteorism in, 451 

milk leg after, 93 

moderate bronchitis in, 451 

mushy stool in, 323 

pain in, 546 

peptonuria in, 360 

phlegmasia alba dolens in, 164 

pleurisy with effusion complicat- 
ing, 235 

recrudescence in, 447 

relapse in, 447 

roseola in, 148, 149, 449 

speech in, 558 

splenic enlargement in, 310 

spontaneous dislocation of the hips 
following, 93 

stools in, 449, 451 

stupor in, 149, 151 

subsultus tendinum in, .">! 

sweating in. 161 

temperature, 447 

tongue in, 113 

tympanites in, 281, 451 

vomiting in, 516 

Widal's test for, 406, 449 

without fever, 449 
Typhomalarial fever. See Malaria, 

remittent. 
Typhus fever, crisis in, 452 

eruption in, 149, 452 

exhaustion in, 452 

fever in, 452 

hematemesis in, 518 

headache in, 452 



Ulcer, duodenal, 292 

of stomach, anemia in, 391 

symptoms of, 291 

vomiting in, 517 
perforating, of foot, 95 
tabetic, of foot, 95 
Ulcers at base of finger nails, 35, 158 
on buccal mucous membrane in 

Schonlein's disease, 126 
on cornea in scrofula, 441 
on tongue, 118 
perforating, in diabetes, senility, and 

tabes dorsalis, 95 
syphilitic, in intestinal tract causing 

diarrhea, 321 
Umbilical hernia, 287, 309 



Uncinaria americana, 327 
anemia due to, 39 1 
duodenale, 327 
Unconsciousness. See Coma. 
Unilateral anesthesia, 171 
facial paralysis, L8. See Paralysis, 
mydriasis, 428 
ptosis, 421 
reflex iridoplegia, significance of, 

427 
wrist-drop, i< 
Uremia. See also Coma, 
amaurosis in. 136. 509 
anemia in, 391 
breath in. 3 

Cheyne-Stokes breathing in. 201 
colliquative diarrhea in, 509 
coma in, 486 

in chronic interstitial nephritis. 
372 
convulsions in, 496, 500 
delirium, mild, 122 
headache in, 471, 472 
hiccough in. 508 
sweating in. hi] 
symptoms of, 486 
tongue in, 114 
vomiting in. 486, 509, 523 
LTreometer, 367 

Urethra, blood in hemorrhage from, 
358 
fever due to passage of sound into, 

446 
gonococci in specific inflammation 

of, 354 
incontinence of urine due to insensi- 
tive, 332 
interference with passage of urine in 
stricture of. 333 
Urethritis, specific gonococci in, 354 
Urecemia. Set Lithemia. 
Uridrosis, 161 
Urine, acetone in. 36} 

Oppenheimer's modification of 
Dennige's test for, 365 
acid fermentation of. 355 
albumin in, boiling test for, 356 
Esbach's method of testing for, 

358 
Heller's test for. 356 
potassium ferrocyanide test for, 

357 
quantitative test for, by centri- 
fuge, 358 
trichloracetic acid test for, 357 
albumose in. 360 
alkaline fermentation of, 355 
bile in. 341. 365 

Gmelin's test for. 341, 365 
stained, in hepatogenous jaundice. 
134 
blood in, 335 



614 



INDEX 



Urine, blood in, test for, 360 
guaiac, 360 
Heller's, 360 
Holland's, 360 
casts in, blood, 346 

epithelial, 345 

fatty, 347 

granular, 346 

hyaline, 347 

of micrococci, 346 

of pus, 346 
chlorides in, 370 

test for, 370 
color of, blue, 339 

brown, 339 

causes of black, 335 
of changes in, 335 

due to blood, 335 

green, 339, 340 

in diabetes, 339 

in iaundice, 339, 340 

red, 335, 339, 340 

white or milky, 339, 340 

yellow, 339 
collecting of, for testing, 333 
crystals in, creatin, 351 

creatinin, 351 

oxalate of lime, 350 

triple phosphates, 350, 352 

urate, 350, 352 

uric acid, 350 
cylindroids in, 348 
diazo-reaction of Ehrlich in, 370 
embryos of parasites in, 353 
epithelial cells in, 353 
fermentation of, 355 
Gmelin's test for bile in, 341, 365 
gonococci in, 354 

guaiacum test for hemoglobin in, 360 
Heller's test for blood in, 360 
in acute diffuse nephritis, 372 
in apoplexy, 332 
in cholera morbus, 316 
in chronic interstitial nephritis, 372 
in diabetes insipidus, 373 

mellitus, 373 
in idiots, 332 
in infectious diseases, 332 
in intestinal obstruction, 514 
in irritation of foreskin or vagina in 

children, 332 
in phosphorus poisoning, 521 
in pyelitis, 342 
in seat-worms, 332 
in some cases of insanity, 332 
in uremia, 486 
incontinence of, 332 
indican in, 341, 365 

test for, 341, 365 
Holland's, 365 
microscopic examination of, 344 
nucleo-albumin in, test for, 358 



Urine, odor of, causes of alteration of, 

334 
oxalates in, 351 
peptone in, 360 

test for, 360 
pus in, 342 

due to calculus, 342 

in pyelitis, 342 

in tuberculosis of kidneys, 342 
quantity of, causes of alteration in, 

334 
retention of, 330 
specific gravity of, 343 
causes of low, 343 
spermatozoa in, 354 
staphylococci and streptococci in, 

354 
Stokvis' modification of .Taffe's test 

for indican in, 365 
sugar in, Fehling's test for, 361 

Haines' test for, 361 

phenylhydrazin test for, 363 

quantitative yeast test of Roberts 
for, 363 

significance of, 363 

Trommer's test for, 363 

Whitney's test for, 361 
total quantity of solids in, Haines' 

modification of Hasser's method 

for computing, 343 
tubercle bacilli in, 353 
urates in, 350 

urea in, amount excreted in health, 
369 

causes of increase and decrease of, 
369, 370 

Lyons' method of estimating, 366 

value of estimating in renal disease 
during pregnancy and before 
surgical operations, 369 
uric acid in, 350 
variations in quantity of, 334 
Urobilin icterus, 134 
Urticaria, 147 
from drugs, 143 
in rheumatism, 143 
of tongue, 119 



Vaccination, eruption of, 153 

roseola following, 146 
Vaccinia, 153 

Vaginitis, specific gonococci in, 354 
Valvular heart disease. See Heart. 
Varicella. See Chickenpox. 
Variola. See Smallpox. 
Vena azygos, thrombosis of, as a cause 

of serous pleural effusion, 236 
Vertigo, 483 

due to drugs, 483 



INDEX 



615 



Vertigo in anemia, 392, 483 

in aortic obstruction, 259 

in apoplexy, 483 

in brain tumors, 483, 509 

in disseminated sclerosis, 483 

in epilepsy, 483 

in indigestion, 483 

in ingravescent apoplexy, 105 

in Meniere's disease, 48? 

in middle-ear disease, 483 

in ocular palsy, 416 

in paretic dementia, 110 

paralyzing, 483 
Vesical crises in locomotor ataxia, 60, 

336, 338 
Vesicular breathing, 219 
Vision, changes in acuity of, 429 

failure of, 429 
Vitiligo, 138 

Vocal fremitus, 204. See Fremitus, 
vocal. 

resonance. See Resonance, vocal. 
Voice, 557 

hoarseness of, 557 

in aneurysm, 557 

in paralysis agitans, 559 

in typhoid fever, 558 

loss of, or mutism, 557 

nasal, causes of, 558 

Avhispering, causes of, 557 
Volvulus, 306, 515 
Vomit, 523 

in cerebral disease, 523 

in intestinal obstruction, 523 

in migraine, 523 

in peritonitis, 523 

in phosphorus poisoning, 523 

in uremia, 523 

in yellow fever, 460 

of chronic gastric catarrh, 519, 523 

of gastric cancer, 290, 509, 517 
dilatation, 519 
ulcer, 517 

of uremia, 509, 523 

test for hemin in. 524 
for sarcinae in, 519 
Vomiting, 508 

associated with headache, 522 

bilious, in remittent malarial fever, 
459 

black, in yellow fever, 460 

centric, from chloroform or ether, 508 

coffee-ground, in gastric cancer, 290, 
517 
in locomotor ataxia, 517 
in phosphorus poisoning, 521 

cyclical, 520 

decrease of urine by persistent, 334 

due to injuries to the epigastrium, 
518 

in acute gastric catarrh, 518 
infectious diseases, 509 



Vomiting in acute gastric miliary tuber- 
culosis, 510 
pancreatitis, 521 
yellow atrophy of liver, 522 
in antimony poisoning, 517 
in apoplexy. 509 
in appendicitis, 516 
in brain abscess, 509" 

tumor, 472, 509 
in catarrhal or obstructive jaun- 
dice, 522 
in cerebellar tumor, 509 
in cerebral anemia, 509 

embolism, 50!) 

hemorrhage, 509 

thrombosis, 509 
in cerebrospinal meningitis, 461 
in cholera Asiatica, 509, 516 

infantum, 316, 517 

morbus, 316, 516 
in chronic gastric catarrh, 519 
in croupous pneumonia, 509 
in diabetes, rarely, 509 
in dilatation of the stomach, 519 
in dysentery, 517 
in early secondary syphilis, 523 
in enterocolitis, not constant, 318 
in erysipelas, 523 
in exophthalmic goitre. 522 
in gastric cancer. 50!). 517 

catarrh, acute, 518 
chronic, 519 

ulcer, 509, 517 
in gastritis, 509, 519 
m hemiplegia due to hematoma of 

dura mater, 109 
in hemoglobinuria. 522 
in hemorrhagic infarction of intes- 
tine, 515 

pressure on brain, 109 
in hepatic abscess, 522 

cirrhosis, 518 

colic, 509 

jaundice, 509 
in hepatitis, 522 
in hysteria, 509, 520 
in influenza, 464 
in ingravescent apoplexy, 105 
in intestinal obstruction, 315, 509, 

511 
in intussusception, 511 
in locomotor ataxia following gas- 
tric crisis. 517 
in melena neonatorum, 518 
in Meniere's disease, 509, 522 
in meningitis, 509, 510 
in merycismus, 523 
in migraine, 522 
in nephritic colic, 509 
in neurasthenia, 520 
in neuroses of stomach, 520 
in peritonitis, 509, 516 



616 



INDEX 



Vomiting in phosphorus poisoning, 521 

in phthisis, 523 

in poisoning by arsenic and anti- 
mony, 517 

in pregnancy, 520 

in profound cerebral anemia, 510 

in pulmonary gangrene, 523 

in purulent meningitis, 510 

in pylephlebitis, 522 

in renal calculus, 522 

in true gastritis, rare, 519 

in typhoid fever, 516 

in uremia, 508, 509 

in whooping-cough, 523 

in yellow fever, 460, 509, 523 

of blood. See Hematemesis. 

uremic, in chronic parenchymatous 
nephritis, 372 
Von Fleischl's hemoglobinometer, 385 



W 



Wandering rash, 120 
Wasting of hand, 40 
"Water-hammer pulse" of aortic regur- 
gitation, 250, 259, 273 / 
Wavy breathing in pneumonia, 203 
"Waxy" casts in urine, 348 
Weil's disease, absence of gastrointes- 
tinal symptoms in, 460 
clay-colored stools in, 460 
fever in, 459 
jaundice in, 133, 460 
swelling of liver and spleen in, 460 
Wernicke's pupil, 428, 473 
Westphal's sign, 60 
Whip-worm, 328 
Whispering voice, 557 
White blood corpuscles, counting of, 
379 
infarct in coronary arteries, 264 
Whitlow, painless, in Morvan's disease, 

44 
Whitney's test for sugar in urine, 361 
Whooping-cough, Cheyne-Stokes respi- 
ration in, 201 
cough in, 525 

hemorrhage of skin in, 142 
ulcer on frenum in, 118 
vomiting in, 523 
Widal's test for typhoid fever, 406 
Williamson's test for sugar in blood, 
408 



Wintrich's change of percussion note in 

tuberculosis, 230 
Word blindness, 560 

deafness, 560 
"Worm-eaten" tongue in mucous dis- 
ease, 115 
Worms, 324 

involuntarv passage of urine due to 
seat-, 332 
Wrist-drop, causes of, 46 
Wrist-jerk, marked, in amyotrophic 

lateral sclerosis, 44 
Wryneck, clonic or tonic, 29 

congenital or acquired, 29 

diagnosis of, 29 

facial asymmetry in connection with, 
16 



Xanthelasma, 117 

Xanthoma, 136 

Xeroderma pigmentosum, 119 



Yellow atrophy of liver, acute, con- 
vulsions in, 504 
coma in, 487 
hematemesis in, 518 
jaundice in, 133 
symptoms of, 134, 522 
fever, black vomit in, 460 
diagnosis of, 460, 461 

between bilious remittent fever 

and, 461 
between dengue and, 460 
fever in, 460 
hematemesis in, 518 
hemorrhage from mucous mem- 
branes in, 460 
jaundice in, 134, 460 
symptoms of, 523 
tarry stools in, 460 
vomiting in, 523 
spot of the eye, 438 



Ziehl's solution for staining tubercle 
bacilli, 534 



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